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CitationGPTRetr11300

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Clinical studies of cerebral blood flow in Alzheimer's disease. Abstract of the paper: Studies of Alzheimer's disease using single-photon emission computed tomography (SPECT) and positron emission tomography (PET) have found reductions in blood flow and glucose metabolism in temporal and parietal cortex. In 50 AD patients who underwent neuropsychological testing and SPECT perfusion imaging, we found significant correlations between perfusion and performance on the Mini-Mental Status Examination in the frontal and parietal lobes. In addition, specific correlations between perfusion in the frontal lobes and performance on tests of frontal lobe ability were noted. These findings, while suggesting the importance of perfusion measures in determining clinical features of the disease, do not clearly define perfusion changes as primary, since similar findings have been seen when metabolism is studied. In a separate group of 5 AD patients and 16 controls, we used PET with the perfusion tracer HIPDM and examined cerebrovascular reactivity to carbon dioxide inhalation. We found that in multiple brain regions, including the temporal lobes, AD patients showed robust and significant increases in perfusion in response to carbon dioxide that did not differ from the response seen in the controls. Taken together, these results show that while perfusion changes are important in AD, they are not clearly either primary or limiting.

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CitationGPTRetr11301

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Altered cerebral energy metabolism in Alzheimer's disease: a PET study. Abstract of the paper: UNLABELLED In an effort to better understand the metabolic basis for the reported decreases in regional cerebral cortex glucose metabolism in patients with Alzheimer's disease, glucose utilization oxygen consumption and regional cerebral blood flow were examined. METHODS Nine patients with Alzheimer's disease and nine age-matched normal controls were imaged using 18F-labeled deoxyglucose and 15O-labeled gases. RESULTS Regional analysis of the cerebral metabolic rate of glucose (CMRglu), cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF) revealed that these values were significantly low in the frontal, parietal and temporal regions. The parietotemporal region had an abnormally high metabolic ratio (CMRO2/CMRglu), while the frontal, sensorimotor and occipital visual cortices had a metabolic ratio similar to that of the normal controls. CONCLUSIONS These findings suggest that the abnormal parietotemporal metabolism in Alzheimer's disease involves a metabolic shift from glycolytic to oxidative metabolism. This impairment of glucose degradation may be the basis for synoptic dysfunction underlying the impairment observed in Alzheimer's disease.

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CitationGPTRetr11302

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Glucose metabolism in normal aging and Alzheimer's disease: Methodological and physiological considerations for PET studies. Abstract of the paper: Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder associated with progressive loss of cognitive function. 2-[18F]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) has long been used to measure resting-state cerebral metabolic rates of glucose, a proxy for neuronal activity. Several FDG PET studies have shown that metabolic reductions occur decades before onset of AD symptoms, suggesting that metabolic deficits may be an upstream event in at least some late-onset AD cases. This review explores this possibility, initially discussing the link between AD pathology, neurodegeneration, oxidative stress and AD, and then discussing findings of FDG PET hypometabolism in AD patients as well as in at-risk individuals, especially those with a first-degree family history of late-onset AD. While the rare early-onset form of AD is due to autosomal dominant genetic mutations, the etiology and pathophysiology of age-dependent, late-onset AD is more complex. Recent FDG PET studies have shown that adult children of AD-affected mothers are more likely than those with AD-fathers to show AD-like brain changes. Given the connection between glucose metabolism and mitochondria, and the fact that mitochondrial DNA is maternally inherited in humans, it is here argued that altered bioenergetics may be an upstream event in those with a maternal history of late-onset AD. Biomarkers of AD have great potential for identifying AD endophenotypes in at-risk individuals, which may help direct investigation of potential susceptibility genes.

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CitationGPTRetr11303

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Abnormalities of energy metabolism in Alzheimer's disease studied with PET. Abstract of the paper: Positron emission tomography (PET) is currently the only technology affording three-dimensional measurement of the brain's energy metabolism which is closely coupled to brain function. Studies of glucose metabolism by PET of (18F)-2-fluoro-2-deoxy-D-glucose are therefore widely applied to show the contribution of various brain structures in the performance of a variety of tasks or their participation in functional deficits associated with various diseases. Although glucose metabolism decreases slightly with age to a regionally different degree, most types of dementia show severe changes in glucose metabolism. Alzheimer's disease (AD) is characterized by metabolic disturbances most prominent in the parietotemporal association cortex and later in the frontal lobe, whereas primary cortical areas, basal ganglia, thalamus, brainstem, and cerebellum are not affected. It is this typical pattern that distinguishes AD from other dementia syndromes. A ratio calculated from the metabolic rates of glucose of "affected" and "nonaffected" brain regions was able to separate patients with AD from age-matched controls and permitted the discrimination of patients with cognitive impairment of other origin in 85%. The discriminative power can be further improved by activation studies. A continuous visual recognition task increased the metabolic rate in normal subjects by 21% and in patients with AD by 6% on average, with significant regional differences. During activation the significant relation between severity of disease and temporoparietal metabolic rate became even stronger. In the assessment of effects of treatment on disturbed metabolism, PET studies demonstrated an equalization of metabolic heterogeneities in patients responding to a muscarinergic cholinagonist, whereas general increases in glucose utilization were observed with piracetam, pyritinol, and phosphatidyl-serine. The therapeutic relevance of such metabolic effects, however, must be proved in controlled clinical trials.

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CitationGPTRetr11304

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Positron emission tomography in Alzheimer's disease. Abstract of the paper: Twenty-one patients with a clinical diagnosis of dementia of the Alzheimer's type (DAT) and 29 healthy, age-matched controls were studied using positron emission tomography (PET) and [18F]2-fluoro-2-deoxy-D-glucose to measure regional cerebral glucose consumption in the resting state. Reductions in ratio measures of relative metabolism in some parietal, temporal, and frontal regions were found in mild, moderate, and severe DAT groups. A significant increase in right/left metabolic asymmetry, particularly in parietal regions, also was seen in mild and moderate groups. Only in the severely demented patients was the absolute cerebral metabolic rate reduced significantly from control values. Fourteen patients had repeated PET studies, but only those patients with moderate to severe dementia showed a decline in IQ over 6 to 15 months. There were no significant changes in metabolic measures over time. PET is useful in quantifying regional cerebral dysfunction in DAT, even in the early stages of the disease.

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CitationGPTRetr11305

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Deficits in cerebral glucose metabolism demonstrated by positron emission tomography in individuals at risk of familial Alzheimer's disease. Abstract of the paper: In order to establish whether positron emission tomography (PET) can identify metabolic changes in Alzheimer's disease at a presymptomatic stage, we have examined 24 asymptomatic at risk individuals from families with Alzheimer's disease. A significant reduction in global cerebral metabolic rate for glucose was found when compared with 16 age-matched controls. There was also a focal, parieto-temporal deficit similar to, although less extensive than, that found in 18 symptomatic individuals from familial Alzheimer's disease (FAD) pedigrees. Follow up of this cohort will establish whether these metabolic changes relate to a presymptomatic stage of the disease.

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CitationGPTRetr11306

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Positron emission tomography in Alzheimer's disease in relation to disease pathogenesis: a critical review. Abstract of the paper: PET studies of brain metabolism and blood flow in Alzheimer's disease (AD) patients lead to the following conclusions: (a) Reductions in "resting state" regional brain metabolism are roughly proportional to dementia severity. (b) These reductions are greater in association than in primary sensory and motor neocortical regions, and correlate with the distribution of neuropathology and cell loss postmortem. (c) Demented but not nondemented Down syndrome adults also have worse metabolic reductions in the association than primary neocortices, suggesting an equivalent pathological process in demented Down syndrome and AD patients. (d) Brain metabolic patterns in AD patients are heterogeneous, belonging to at least four distinct metabolic groups that correspond to different patterns of cognitive and behavioral abnormalities; the metabolic patterns have not been shown to be related to disease etiology. (e) Abnormal right-left metabolic asymmetries in mildly demented AD patients can retain their initial directions for as long as 48 months; these asymmetries precede and predict the cognitive "discrepancies" that later appear, such that moderately demented patients with disproportionate visuospatial compared with language deficits, or disproportionate visual recall compared with verbal recall, have a greater metabolic reduction in the right than left hemisphere, and vice versa. (f) Parietal association/frontal association metabolic ratios also retain their direction over time; in moderately demented patients, relative hypometabolism in the prefrontal association cortex is related to deficits in verbal fluency and attention to simple sets, whereas relative hypometabolism in the parietal association cortex correlates with failure in arithmetic, verbal comprehension, drawing, and immediate memory for visuospatial location. (g) Although metabolically spared compared with the association cortices, the primary sensory cortices, basal ganglia, thalamus, and cerebellar hemispheres show metabolic declines in AD using high-resolution PET scanners, possibly due to their connections with more pathologically affected regions. (h) Early metabolic deficits in AD are hypothesized to arise from synaptic failure in association cortical areas; such failure in the occipitotemporal visual cortex can be reversed in mildly to moderately demented AD patients who are capable of performing a face-matching task.

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CitationGPTRetr11307

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: PET approaches for diagnosis of dementia. Abstract of the paper: There is increasing use of neuroimaging modalities, including PET, for diagnosing dementia. For example, FDG-PET demonstrates hypometabolic regions in the posterior cingulate gyri, precuneus, and parietotemporal association cortices, while amyloid PET indicates amyloid deposition in Alzheimer disease and mild cognitive impairment due to Alzheimer disease. Furthermore, the use of combination PET with structural MR imaging can improve the diagnostic accuracy of dementia. In other neurodegenerative dementias, each disease exhibits a specific metabolic reduction pattern. In dementia with Lewy bodies, occipital glucose metabolism is decreased, while in frontotemporal dementia, frontal and anterior temporal metabolism is predominantly decreased. These FDG-PET findings and positive or negative amyloid deposits are important biomarkers for various neurodegenerative dementias.

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CitationGPTRetr11308

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Imaging studies and APOE genotype in persons at risk for Alzheimer's disease. Abstract of the paper: Many studies have investigated APOE-related differences in cerebral structure, blood flow, metabolism, and activation in an attempt to detect early brain changes in subjects at risk for Alzheimer's disease (AD). Structural magnetic resonance imaging studies have produced conflicting results, with some failing to detect APOE-related differences and others suggesting that epsilon4 carriers have more pronounced atrophy, particularly at medial temporal structures. All functional imaging studies done during rest in middle-aged and elderly subjects have found decreased cerebral metabolism for epsilon4 carriers (mostly in areas that usually are affected by AD), and some have reported faster cerebral metabolic reductions over time. Areas with decreased resting cerebral perfusion and metabolism, in addition to other areas with increased perfusion, have been reported in young epsilon4 carriers. Imaging studies done during the performance of various cognitive tasks in middle-aged and elderly subjects, and a single study in young subjects, have produced mixed results with regionally nonspecific increased, decreased, or nondifferential APOE-related activations depending on the cognitive task used. APOE-related findings in imaging studies of nondemented subjects may be the result of incipient AD pathologic changes or of genetic heterogeneity in brain structure and function.

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CitationGPTRetr11309

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Brain glucose hypometabolism and oxidative stress in preclinical Alzheimer's disease. Abstract of the paper: One of the main features of Alzheimer's disease (AD) is the severe reduction of the cerebral metabolic rate for glucose (CMRglc). In vivo imaging using positron emission tomography with 2-[(18)F]fluoro-2-deoxy-D-glucose (FDG-PET) demonstrates consistent and progressive CMRglc reductions in AD patients, the extent and topography of which correlate with symptom severity. Increasing evidence suggests that CMRglc reductions occur at the preclinical stages of AD. CMRglc reductions were observed on FDG-PET before the onset of disease in several groups of at-risk individuals, including patients with mild cognitive impairment (MCI), often a prodrome to AD; presymptomatic individuals carrying mutations responsible for early-onset familial AD; cognitively normal elderly individuals followed for several years until they declined to MCI and eventually to AD; normal, middle-aged individuals who expressed subjective memory complaints and were carriers of the apolipoprotein E epsilon-4 allele, a strong genetic risk factor for late-onset AD. However, the causes of the early metabolic dysfunction forerunning the onset of AD are not known. An increasing body of evidence indicates a deficient or altered energy metabolism that could change the overall oxidative microenvironment for neurons during the pathogenesis and progression of AD, leading to alterations in mitochondrial enzymes and in glucose metabolism in AD brain tissue. The present paper reviews findings that implicate hypometabolism and oxidative stress as crucial players in the initiation and progression of synaptic pathology in AD.

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CitationGPTRetr11310

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Greater metabolic rate decreases in hippocampal formation and proisocortex than in neocortex in Alzheimer's disease. Abstract of the paper: Neuropathological studies of Alzheimer's disease (AD) have found pathological changes in some cytoarchitectural regions and relative sparing in others. Positron emission tomography (PET) studies have also shown selective decreases in glucose metabolic rates but have generally focused on whole brain lobes or geometrically derived regions of interest. In this report, a template of Brodmann areas, derived from a whole brain histological section atlas, was used to analyze PET findings from 34 AD patients and 16 control subjects matched for age, sex, and educational level. AD patients had lowest glucose metabolic rates in limbic areas of the temporal lobe and other proisocortical areas higher rates in frontal lobe and unimodal association areas, and relative sparing of parietal/occipital lobes and motor/sensory cortices. Analysis of variance revealed larger effect sizes when AD and control subjects were compared on metabolic rate for cortical type than for lobe. These findings, which parallel neuropathological studies of regional distribution of neurofibrillary tangles in AD, suggest that vulnerability is greatest in cortical areas that are in closer synaptic contact with limbic areas.

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CitationGPTRetr11311

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: PET imaging in the assessment of normal and impaired cognitive function. Abstract of the paper: PET has been used to directly quantify several processes relevant to the status of cerebral health and function, including cerebral blood flow, cerebral blood volume, cerebral rate of oxygen metabolism, and cerebral glucose use. Clinically, the most commonly performed PET studies of the brain are performed with fluorine-18-fluorodeoxyglucose as the imaged radiopharmaceutical. Such scans have demonstrated diagnostic and prognostic use in evaluating patients who have cognitive impairment, and in distinguishing among primary neurodegenerative dementias and other causes of cognitive decline. In certain pathologic circumstances, the normal coupling between blood flow and metabolic needs may be disturbed, and changes in oxygen extraction fraction can have significant prognostic value.

False

CitationGPTRetr11312

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Longitudinal PET Evaluation of Cerebral Metabolic Decline in Dementia: A Potential Outcome Measure in Alzheimer's Disease Treatment Studies. Abstract of the paper: OBJECTIVE It is well established that regional cerebral metabolic rates for glucose assessed by [(18)F]fluorodeoxyglucose (FDG) positron emission tomography (PET) in patients with Alzheimer's disease in the mental resting state (eyes and ears covered) provide a sensitive, in vivo metabolic index of Alzheimer's disease dementia. Few studies, however, have evaluated longitudinal declines in regional cerebral glucose metabolism in patients with dementia caused by Alzheimer's disease. In addition, the available studies have not used recently developed brain mapping algorithms to characterize the progression of Alzheimer's disease throughout the brain, and none considered the statistical power of regional cerebral glucose metabolism in testing the ability of treatments to attenuate the progression of dementia. METHOD The authors used FDG PET and a brain mapping algorithm to investigate cross-sectional reductions in regional cerebral glucose metabolism, longitudinal decline in regional cerebral glucose metabolism after a 1-year follow-up, and the power of this method to evaluate treatments for Alzheimer's disease in patients with mild to moderate dementia. PET scans were initially acquired in 14 patients with Alzheimer's disease and 34 healthy comparison subjects of similar age and sex. Repeat scans were obtained in the patients 1 year later. Power analyses for voxels showing maximal decline over the 1-year period in regional cerebral glucose metabolism (mg/100 g per minute) were computed to estimate the sample sizes needed to detect a significant treatment response in a 1-year, double-blind, placebo-controlled treatment study. RESULTS The patients with Alzheimer's disease had significantly lower glucose metabolism than healthy comparison subjects in parietal, temporal, occipital, frontal, and posterior cingulate cortices. One year later, the patients with Alzheimer's disease had significant declines in glucose metabolism in parietal, temporal, frontal, and posterior cingulate cortices. Using maximal glucose metabolism reductions in the left frontal cortex, we estimated that as few as 36 patients per group would be needed to detect a 33% treatment response with one-tailed significance of p</=0.005 and 80% power in a 1-year, double-blind, placebo-controlled treatment study. CONCLUSIONS These findings indicate that brain metabolism as assessed by FDG PET during mental rest is a sensitive marker of disease progression in Alzheimer's disease over a 1-year period. These findings also support the feasibility of using FDG PET as an outcome measure to test the ability of treatments to attenuate the progression of Alzheimer's disease.

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CitationGPTRetr11313

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Oxidative energy metabolism in Alzheimer brain. Studies in early-onset and late-onset cases. Abstract of the paper: Reduction of the cerebral metabolic rate of glucose is one of the most predominant abnormalities generally found in the Alzheimer brain, whereas the cerebral metabolic rate of oxygen is only slightly diminished or not at all the beginning of this dementive disorder. This metabolic abnormality may induce severe functional disturbances, obviously preceding morphobiological changes. From the cerebral metabolic rates of oxidized glucose and oxygen, the cerebral ATP formation rate was calculated in incipient early-onset, incipient late-onset and stable advanced dementia of Alzheimer type. A reduction of ATP formation was found from at least 7% in incipient early-onset, to around 20% in incipient late-onset DAT, and from 35% to more than 50% in stable advanced dementia. This approximation was adjusted to findings demonstrating diminished activities of enzymes active in glucose metabolism and formation of oxidation equivalents for ATP production from substrates other than glucose. A reduction for energy formation to the same range was found, as was also recently reported, in vivo in Alzheimer patients. From this rather theoretical point of view, a permanent loss of energy by at least 7-20% in incipient and progressively advancing dementia of the Alzheimer type may be assumed, with an increasing tendency in stable advanced dementia to around 50% energy loss. This energy deficit may have drastic impacts on brain function.

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CitationGPTRetr11314

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Intercorrelations of regional cerebral glucose metabolic rates in Alzheimer's disease. Abstract of the paper: Patterns of cerebral metabolic correlations were compared between 21 Alzheimer's disease patients and 21 healthy age-matched controls in the resting state. Cerebral metabolic rates for glucose were determined by positron emission tomography using [18F]2-fluoro-2-deoxy-D-glucose. Partial correlation coefficients, controlling for whole brain glucose metabolism, were evaluated between pairs of regional glucose metabolic rates in 59 brain regions. Reliable correlation coefficients were obtained with the 'jackknife' and 'bootstrap' statistical procedures. Compared with healthy controls, the Alzheimer patients had significantly fewer reliable partial correlation coefficients between frontal and parietal lobe regions, and more reliable correlations between the cerebellum and temporal lobe. The number of reliable correlations between many bilaterally symmetric brain regions was reduced in the Alzheimer patients, as compared with controls. These results suggest that in the early stages of Alzheimer's disease there is a breakdown of the organized functional activity between the two cerebral hemispheres, and between parietal and frontal lobe structures.

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CitationGPTRetr11315

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: PET studies in dementia. Abstract of the paper: Measurement of local cerebral glucose metabolism (lCMRGlc) by positron emission tomography (PET) and 18F-2-fluoro-2-deoxy-D-glucose (FDG) has become a standard technique during the past 20 years and is now available at many university hospitals in all highly developed countries. Many studies have documented a close relation between lCMRGlc and localized cognitive functions, such as language and visuoconstructive abilities. Alzheimer's disease (AD) is characterized by regional impairment of cerebral glucose metabolism in neocortical association areas (posterior cingulate, temporoparietal and frontal multimodal association cortex), whereas primary visual and sensorimotor cortex, basal ganglia, and cerebellum are relatively well preserved. In a multicenter study comprising 10 PET centers (Network for Efficiency and Standardisation of Dementia Diagnosis, NEST-DD) that employed an automated voxel-based analysis of FDG PET images, the distinction between controls and AD patients was 93% sensitive and 93% specific, and even in very mild dementia (at MMSE 24 or higher) sensitivity was still 84% at 93% specificity. Significantly abnormal metabolism in mild cognitive deficit (MCI) indicates a high risk to develop dementia within the next two years. Reduced neocortical glucose metabolism can probably be detected with FDG PET in AD on average one year before onset of subjective cognitive impairment. In addition to glucose metabolism, specific tracers for dopamine synthesis (18F-F-DOPA) and for (11C-MP4A) are of interest for differentiation among dementia subtypes. Cortical acetylcholine esterase activity (AChE) activity is significantly lower in patients with AD or with dementia with Lewy bodies (DLB) than in age-matched normal controls. In LBD there is also impairment of dopamine synthesis, similar to Parkinson disease.

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CitationGPTRetr11316

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Cortical abnormalities in Alzheimer's disease. Abstract of the paper: Regional cerebral glucose metabolism, an index of neuronal activity, was compared in 20 patients with Alzheimer's disease and 8 age-matched normal volunteers by positron emission tomography following [18F]2-fluoro-2-deoxy-D-glucose administration. Overall cortical glucose utilization in the Alzheimer's group was 10 to 49% below that of control individuals. The posterior parietal cortex and contiguous portions of posterior temporal and anterior occipital lobes were most severely affected; frontal cortex was relatively spared. This pattern of cortical involvement is consistent with the major clinical features of Alzheimer's disease. Comparison of patients with early and more advanced dementia suggested that a substantial decline in glucose metabolism occurs before cognitive impairment becomes evident; once the patient is symptomatic, however, small additional metabolic decrements are associated with a marked deterioration in intellectual function.

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CitationGPTRetr11317

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Functional imaging patterns in Alzheimer's disease. Relationships to neurobiology. Abstract of the paper: Brain imaging with functional techniques, such as positron emission tomography (PET) and single photon emission computed tomography (SPECT) have been widely applied to the study of dementia. While the pattern of temporal and parietal hypometabolism and hypoperfusion have often been suggested to be of diagnostic utility in ascertaining that a dementia is due to Alzheimer's disease (AD), the exact sensitivity and specificity of this pattern in clinically important situations is unclear. These imaging findings have been of considerable interest, however, in describing the regional patterns of predilection in the disease. Evidence supports the contention that the earliest sites of functional impairment in AD are in the temporal lobes. Surprisingly, however, mesial temporal lobe hypometabolism was difficult to detect in a group of mildly demented AD patients in comparison to a group of healthy older subjects. These results suggest that simple use of mesial temporal lobe metabolic rates as a diagnostic for AD may not be fruitful, and that evaluation of the earliest stages of AD can be most productively studied by investigating healthy older individuals.

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CitationGPTRetr11318

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Predominant left hemisphere metabolic dysfunction in dementia. Abstract of the paper: Thirty-one patients with probable Alzheimer's disease and 11 patients with memory disorders, attributable to multiple cerebral infarctions, were studied using 18-F-fluorodeoxyglucose-positron emission tomography scans. Asymmetry in cerebral glucose metabolism within these diagnostic groups was assessed by comparison with the metabolic rates obtained in age-equivalent healthy control subjects. A significantly greater number of individuals in both patient groups exhibited predominant left rather than right hemisphere hypometabolism. In addition, for patients with Alzheimer's disease, the degree of asymmetry was not related to either the severity or duration of dementia. These findings could be explained by greater susceptibility of the left hemisphere to degenerative or ischemic brain disease, by a specific sampling effect, or most likely, by greater metabolic deficits resulting from left rather than right hemisphere impairment.

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CitationGPTRetr11319

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: for example previous studies using pet and single photon emission computed tomography techniques found that ad patients had abnormally low cerebral blood flow and low cerebral metabolic rates for glucose in many brain regions including the parietal temporal and prefrontal cortices and the pcc Title of the paper: Functional imaging of cognition in Alzheimer's disease using positron emission tomography. Abstract of the paper: Positron emission tomography in Alzheimer's disease (AD) demonstrates a metabolic decrease, predominantly in associative posterior cortices (comprising the posterior cingulate cortex), and also involving medial temporal structures and frontal regions at a lesser degree. The level of activity in this wide network is roughly correlated with dementia severity, but several confounds (such as age, education or subcortical ischemic lesions) may influence the brain-behaviour relationship. Univariate analyses allow one to segregate brain regions that are particularly closely related to specific neuropsychological performances. For example, a relationship was established between the activity in lateral associative cortices and semantic performance in AD. The role of semantic capacities (subserved by temporal or parietal regions) in episodic memory tasks was also emphasized. The residual activity in medial temporal structures was related to episodic memory abilities, as measured by free recall performance, cued recall ability and recognition accuracy. More generally, AD patients' performance on episodic memory tasks was correlated with the metabolism in several structures of Papez's circuit (including the medial temporal and posterior cingulate regions). Multivariate analyses should provide complementary information on impaired metabolic covariance in functional networks of brain regions and the consequences for AD patients' cognitive performance. More longitudinal studies are being conducted that should tell us more about the prognostic value of initial metabolic impairment and the neural correlates of progressive deterioration of cognitive performance in AD.

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CitationGPTRetr11320

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress. Abstract of the paper: Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Abeta) peptides. Although the disease undoubtedly reflects the interaction of complex multifactorial processes, Abeta itself is toxic to neurons in vitro and the load of Abeta in vivo correlates well with the degree of cognitive impairment. There has therefore been considerable interest in the mechanism(s) of Abeta neurotoxicity. We here review the basic biology of Abeta processing and consider some of the major areas of focus of this research. It is clear that both AD and Abeta toxicity are characterized by oxidative stress, alterations in the activity of enzymes of intermediary metabolism, and mitochondrial dysfunction, especially impaired activity of cytochrome c oxidase. Studies in vitro also show alterations in cellular calcium signaling. We consider the mechanisms proposed to mediate cell injury and explore evidence to indicate which of these many changes in function are primary and which secondary.

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CitationGPTRetr11321

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta-peptide impairs ion-motive ATPase activities: evidence for a role in loss of neuronal Ca2+ homeostasis and cell death. Abstract of the paper: The amyloid beta-peptide (A beta) that accumulates as insoluble plaques in the brain in Alzheimer's disease can be directly neurotoxic and can increase neuronal vulnerability to excitotoxic insults. The mechanism of A beta toxicity is unclear but is believed to involve generation of reactive oxygen species (ROS) and loss of calcium homeostasis. We now report that exposure of cultured rat hippocampal neurons to A beta 1-40 or A beta 25-35 causes a selective reduction in Na+/K(+)-ATPase activity which precedes loss of calcium homeostasis and cell degeneration. Na+/K(+)-ATPase activity was reduced within 30 min of exposure to A beta 25-35 and declined to less than 40% of basal level by 3 hr. A beta did not impair other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. Experiments with ouabain, a specific inhibitor of the Na+/K(+)-ATPase, demonstrated that impairment of this enzyme was sufficient to induce an elevation of [Ca2+]i and neuronal injury. Impairment of Na+/K(+)-ATPase activity appeared to be causally involved in the elevation of [Ca2+]i and neurotoxicity since suppression of Na+ influx significantly reduced A beta- and ouabain-induced [Ca2+]i elevation and neuronal death. Neuronal degeneration induced by ouabain appeared to be of an apoptotic form as indicated by nuclear condensation and DNA fragmentation. The antioxidant free radical scavengers vitamin E and propylgallate significantly attenuated A beta-induced impairment of Na+/K(+)-ATPase activity, elevation of [Ca2+]i and neurotoxicity, suggesting a role for ROS. Finally, exposure of synaptosomes from postmortem human hippocampus to A beta resulted in a significant and specific reduction in Na+/K(+)-ATPase and Ca(2+)-ATPase activities, without affecting other Mg(2+)-dependent ATPase activities or Na+/Ca2+ exchange. These data suggest that impairment of ion-motive ATPases may play a role in the pathogenesis of neuronal injury in Alzheimer's disease.

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CitationGPTRetr11322

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta-peptide induces cholinergic dysfunction and cognitive deficits: a minireview. Abstract of the paper: Amyloid beta-peptide (Abeta) plays a critical role in the development of Alzheimer's disease (AD). Much progress has been made in understanding this age-related neurodegenerative disorder, thus an insight into the cellular actions of Abeta and resulting functional consequences may contribute to preventive and therapeutic approaches for AD. In this review, recent evidence of Abeta-induced brain dysfunction, particularly of cholinergic impairment and memory deficits is summarized. Moreover, proposed mechanisms for Abeta-induced neurotoxicity such as oxidative stress, ion-channel formation, and Abeta-receptor interaction are discussed.

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CitationGPTRetr11323

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain. Abstract of the paper: Oxidative stress is extensive in Alzheimer disease (AD) brain. Amyloid beta-peptide (1-42) has been shown to induce oxidative stress and neurotoxicity in vitro and in vivo. Genetic mutations that result in increased production of Abeta1-42 from amyloid precursor protein are associated with an early onset and accelerated pathology of AD. Consequently, Abeta1-42 has been proposed to play a central role in the pathogenesis of AD as a mediator of oxidative stress. In this review, we discuss the role of Abeta1-42 in the lipid peroxidation and protein oxidation evident in AD brain and the implications of such oxidative stress for the function of various proteins that we have identified as specifically oxidized in AD brain compared to control, using proteomics methods. Additionally, we discuss the critical role of methionine 35 in the oxidative stress and neurotoxic properties exhibited by Abeta1-42.

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CitationGPTRetr11324

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Calcium signals induced by amyloid beta peptide and their consequences in neurons and astrocytes in culture. Abstract of the paper: In Alzheimer's disease, amyloid beta (Abeta) peptide is deposited in neuritic plaques in the brain. The Abeta peptide 1-42 or the fragment 25-35 are neurotoxic. We here review our recent explorations of the mechanisms of Abeta toxicity in hippocampal cultures. Abeta had no effect on intracellular calcium in neurons but caused striking changes in nearby astrocytes. The [Ca(2+)](c) signals started approximately 5-15 min after Abeta application and consisted of sporadic [Ca(2+)](c) pulses. These were entirely dependent on extracellular Ca(2+), independent of ER Ca(2+) stores and resulted from Ca(2+) influx, probably through Abeta-induced membrane channels. The Ca(2+) signals were closely associated with transient, episodic acidification which may reflect displacement of protons from binding sites or Ca(2+)/2H(+) exchange. Abeta caused an increased rate of generation of reactive oxygen species (ROS), also seen in astrocytes and not in neurons. The increased ROS generation was blocked by inhibitors of the NADPH oxidase, strongly suggesting that this enzyme, normally associated with immune cells, is expressed in astrocytes. ROS generation was also Ca(2+)-dependent, suggesting that Abeta activation of the enzyme may be secondary to the increase in [Ca(2+)](c). Abeta caused delayed neuronal death despite the fact that all responses were seen only in astrocytes. Neurons could not be protected by glutamate receptor antagonists, but were rescued by inhibition of the NADPH oxidase, by antioxidants and by increasing glutathione. These data suggest that Abeta causes Ca(2+)-dependent oxidative stress by activating an astrocytic NADPH oxidase, and that neuronal death follows through a failure of antioxidant support.

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CitationGPTRetr11325

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta peptide of Alzheimer's disease downregulates Bcl-2 and upregulates bax expression in human neurons. Abstract of the paper: Neuronal apoptosis is a suspected cause of neurodegeneration in Alzheimer's disease (AD). Increased levels of amyloid beta peptide (Abeta) induce neuronal apoptosis in vitro and in vivo. The underlying molecular mechanism of Abeta neurotoxicity is not clear. The normal concentration of Abeta in cerebrospinal fluid is 4 nM. We treated human neuron primary cultures with 100 nM amyloid beta peptides Abeta(1-40) and Abeta(1-42) and the control reverse peptide Abeta(40-1). We find that although little neuronal apoptosis is induced by either peptide after 3 d of treatment, Abeta(1-42) provokes a rapid and sustained downregulation of a key anti-apoptotic protein, bcl-2, whereas it increases levels of bax, a protein known to promote cell death. In contrast, the Abeta(1-40) downregulation of bcl-2 is gradual, although the levels are equivalent to those of Abeta(1-42)-treated neurons by 72 hr of treatment. Abeta(1-40) does not upregulate bax levels. The control, reverse peptide Abeta(40-1), does not affect either bcl-2 or bax protein levels. In addition, we found that the Abeta(1-40)- and Abeta(1-42)- but not Abeta(40-1)-treated neurons had increased vulnerability to low levels of oxidative stress. Therefore, we propose that although high physiological amounts of Abeta are not sufficient to induce apoptosis, Abeta depletes the neurons of one of its anti-apoptotic mechanisms. We hypothesize that increased Abeta in individuals renders the neurons vulnerable to age-dependent stress and neurodegeneration.

False

CitationGPTRetr11326

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Alzheimer's amyloid beta-peptide (1-42) induces cell death in human neuroblastoma via bax/bcl-2 ratio increase: an intriguing role for methionine 35. Abstract of the paper: The beta amyloid (Abeta), the major protein component of brain senile plaques in Alzheimer's disease, is known to be directly responsible for the production of free radicals toxic to brain tissue and the redox state of Met-35 residue seems to play a particular and critical role in peptide's neurotoxic actions. In this study, we investigated, in human neuroblastoma cells (IMR-32), the relationship between the oxidative state of methionine, and both neurotoxic and pro-apoptotic actions induced by Abeta-peptide, comparing the effects of native peptide, in which the Met-35 is present in the reduced state, with those of a modified peptide with oxidized Met-35 (Abeta(1-42)(35Met-ox)), as well as an Abeta-derivative with Met-35 substituted with norleucine (Abeta(1-42)(35Nle)). The obtained results show that Abeta induces a time-dependent decrease in cell viability; Abeta(1-42)(35Met-ox) was significantly less potent, though inducing a remarkable decrease in cell viability compared to control. On the contrary, no toxic effects were observed after treatment with Abeta(1-42)(35Nle). Abeta-peptide as well as the amyloid modified peptide with oxidized Met-35 induced the pro-apoptotic gene bax over-expression after 24 h, whereas Abeta(1-42)(35Nle) had no effect. Conversely, bcl-2, an anti-apoptotic gene, became highly down-regulated by Abeta peptide treatment, in contrast to that evidenced by the Abeta(1-42)(35Met-ox) peptide. Finally, Abeta caused an increase in caspase-3 activity to be higher with respect to that shown by Abeta(1-42)(35Met-ox) while Abeta(1-42)(35Nle) had no effect. These results support the hypothesis that Abeta-induced neurotoxicity occurs via bax over-expression, bcl-2 down-regulation, and caspase-3 activation, first indicating that methionine 35 redox state may alter this cell death pathway.

False

CitationGPTRetr11327

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta-peptide and oxidative cellular injury in Alzheimer's disease. Abstract of the paper: Alzheimer's disease is a progressive neurodegenerative disorder that affects primarily learning and memory functions. There is significant neuronal loss and impairment of metabolic functioning in the temporal lobe, an area believed to be crucial for learning and memory tasks. Aggregated deposits of amyloid beta-peptide may have a causative role in the development and progression of AD. We review the cellular actions of A beta and how they can contribute to the cytotoxicity observed in AD. A beta causes plasma membrane lipid peroxidation, impairment of ion-motive ATPases, glutamate uptake, uncoupling of a G-protein linked receptor, and generation of reactive oxygen species. These effects contribute to the loss of intracellular calcium homeostasis reported in cultured neurons. Many cell types other than neurons show alterations in the Alzheimer's brain. The effects of A beta on these cell types is also reviewed.

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CitationGPTRetr11328

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease. Abstract of the paper: Perturbed neuronal Ca(2+) homeostasis is implicated in age-related cognitive impairment and Alzheimer's disease (AD). With advancing age, neurons encounter increased oxidative stress and impaired energy metabolism, which compromise the function of proteins that control membrane excitability and subcellular Ca(2+) dynamics. Toxic forms of amyloid beta-peptide (Abeta) can induce Ca(2+) influx into neurons by inducing membrane-associated oxidative stress or by forming an oligomeric pore in the membrane, thereby rendering neurons vulnerable to excitotoxicity and apoptosis. AD-causing mutations in the beta-amyloid precursor protein and presenilins can compromise these normal proteins in the plasma membrane and endoplasmic reticulum, respectively. Emerging knowledge of the actions of Ca(2+) upstream and downstream of Abeta provides opportunities to develop novel preventative and therapeutic interventions for AD.

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CitationGPTRetr11329

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta-peptide is produced by cultured cells during normal metabolism. Abstract of the paper: Alzheimer's disease is characterized by the extracellular deposition in the brain and its blood vessels of insoluble aggregates of the amyloid beta-peptide (A beta), a fragment, of about 40 amino acids in length, of the integral membrane protein beta-amyloid precursor protein (beta-APP). The mechanism of extracellular accumulation of A beta in brain is unknown and no simple in vitro or in vivo model systems that produce extracellular A beta have been described. We report here the unexpected identification of the 4K (M(r) 4,000) A beta and a truncated form of A beta (approximately 3K) in media from cultures of primary cells and untransfected and beta-APP-transfected cell lines grown under normal conditions. These peptides were immunoprecipitated readily from culture medium by A beta-specific antibodies and their identities confirmed by sequencing. The concept that pathological processes are responsible for the production of A beta must not be reassessed in light of the observation that A beta is produced in soluble form in vitro and in vivo during normal cellular metabolism. Further, these findings provide the basis for using simple cell culture systems to identify drugs that block the formation or release of A beta, the primary protein constituent of the senile plaques of Alzheimer's disease.

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CitationGPTRetr11330

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Mitochondria and Alzheimer's disease: amyloid-beta peptide uptake and degradation by the presequence protease, hPreP. Abstract of the paper: Several lines of evidence suggest mitochondrial dysfunction as a possible underlying mechanism of Alzheimer's disease (AD). Accumulation of the amyloid-beta peptide (Abeta), a neurotoxic peptide implicated in the pathogenesis of AD, has been detected in brain mitochondria of AD patients and AD transgenic mouse models. In vitro evidence suggests that the Abeta causes mitochondrial dysfunction e.g. oxidative stress, mitochondrial fragmentation and decreased activity of cytochrome c oxidase and TCA cycle enzymes. Here we review the link between mitochondrial dysfunctions and AD. In particular we focus on the mechanism for Abeta uptake by mitochondria and on the recently identified Abeta degrading protease in human brain mitochondria.

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CitationGPTRetr11331

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Cellular mechanisms of beta-amyloid production and secretion. Abstract of the paper: The major constituent of senile plaques in Alzheimer's disease is a 42-aa peptide, referred to as beta-amyloid (Abeta). Abeta is generated from a family of differentially spliced, type-1 transmembrane domain (TM)-containing proteins, called APP, by endoproteolytic processing. The major, relatively ubiquitous pathway of APP metabolism in cell culture involves cleavage by alpha-secretase, which cleaves within the Abeta sequence, thus precluding Abeta formation and deposition. An alternate secretory pathway, enriched in neurons and brain, leads to cleavage of APP at the N terminus of the Abeta peptide by beta-secretase, thus generating a cell-associated beta-C-terminal fragment (beta-CTF). A pathogenic mutation at codons 670/671 in APP (APP "Swedish") leads to enhanced cleavage at the beta-secretase scissile bond and increased Abeta formation. An inhibitor of vacuolar ATPases, bafilomycin, selectively inhibits the action of beta-secretase in cell culture, suggesting a requirement for an acidic intracellular compartment for effective beta-secretase cleavage of APP. beta-CTF is cleaved in the TM domain by gamma-secretase(s), generating both Abeta 1-40 (90%) and Abeta 1-42 (10%). Pathogenic mutations in APP at codon 717 (APP "London") lead to an increased proportion of Abeta 1-42 being produced and secreted. Missense mutations in PS-1, localized to chromosome 14, are pathogenic in the majority of familial Alzheimer's pedigrees. These mutations also lead to increased production of Abeta 1-42 over Abeta 1-40. Knockout of PS-1 in transgenic animals leads to significant inhibition of production of both Abeta 1-40 and Abeta 1-42 in primary cultures, indicating that PS-1 expression is important for gamma-secretase cleavages. Peptide aldehyde inhibitors that block Abeta production by inhibiting gamma-secretase cleavage of beta-CTF have been discovered.

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CitationGPTRetr11332

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Cell degeneration induced by amyloid-beta peptides: implications for Alzheimer's disease. Abstract of the paper: Extracellular accumulation of amyloid-beta (Abeta) peptide and death of neurons in brain regions involved in learning and memory, particularly the cortex and the hippocampus, are central features of Alzheimer's disease (AD). Neuronal Ca2+ overload and apoptosis are known to occur in AD. Abeta might play a role in disrupting Ca2+ homeostasis, and this AD-associated amyloidogenic peptide has been reported to induce apoptotic death in cultured cells. However, the specific intracellular signaling pathways by which Abeta triggers cell death are not yet well defined. This article provides evidence for the involvement of mitochondrial dysfunction in Abeta-induced toxicity and for the role of mitochondria in apoptosis triggered by Abeta. In addition, the endoplasmic reticulum (ER) seems to play a role in Abeta-induced apoptotic neuronal death, the ER stress being mediated by the perturbation of ER Ca2+ homeostasis. It is likely that a better understanding of how Abeta induces neuronal apoptosis will lead to the identification of potential molecular targets for the development of therapies for AD.

False

CitationGPTRetr11333

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: New insights in the amyloid-Beta interaction with mitochondria. Abstract of the paper: Biochemical and morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer's disease (AD). Particularly, mitochondrial dysfunction is a hallmark of amyloid-beta-induced neuronal toxicity in Alzheimer's disease. The recent emphasis on the intracellular biology of amyloid-beta and its precursor protein (APP) has led researchers to consider the possibility that mitochondria-associated and mitochondrial amyloid-beta may directly cause neurotoxicity. Both proteins are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron transport chain, increase reactive oxygen species production, cause mitochondrial damage, and prevent neurons from functioning normally. In this paper, we will outline current knowledge of the intracellular localization of amyloid-beta. Moreover, we summarize evidence from AD postmortem brain as well as animal AD models showing that amyloid-beta triggers mitochondrial dysfunction through a number of pathways such as impairment of oxidative phosphorylation, elevation of reactive oxygen species production, alteration of mitochondrial dynamics, and interaction with mitochondrial proteins. Thus, this paper supports the Alzheimer cascade mitochondrial hypothesis such as the most important early events in this disease, and probably one of the future strategies on the therapy of this neurodegenerative disease.

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CitationGPTRetr11334

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: A beta peptides and calcium influence secretion of the amyloid protein precursor from chick sympathetic neurons in culture. Abstract of the paper: The major constituent of amyloid plaques in the Alzheimer disease (AD) brain is the amyloid protein (A beta). A beta has been shown to be neurotoxic to cells, but the exact mechanism of its effects are still not known. Most studies have focussed on A beta neurotoxicity, but little is known about the effect of A beta peptides on cellular protein metabolism and secretion. To examine the effect of A beta peptides on APP secretion, chick sympathetic neurons were metabolically labeled with [(35)S]methionine and the amounts of radiolabeled APP and A beta quantitated. Several A beta peptides (A beta(25-35), [pyroglu(3)]A beta(3-40), and [pyroglu(11)]A beta(11-40)) inhibited secretion of [(35)S]APP and increased cell-associated [(35)S]APP. There was also a 2-2.5-fold increase in secretion of several other proteins when cells were incubated with A beta(25-35). However, the amount of A beta secreted into the medium was decreased. Treatment of cells with the calcium ionophore A23187 caused a 1.5-fold increase in secreted [(35)S]APP and a decrease in cell-associated [(35)S]APP. Although L-type voltage-dependent calcium channels (VDCC) have been implicated in A beta toxicity, the effect of L-type VDCC on APP secretion has not previously been examined. The L-type VDCC antagonists nifedipine and diltiazem both increased [(35)S]APP secretion into the medium but did not influence the effect of A beta on [(35)S]APP secretion. These studies suggest that A beta interferes with the secretory pathway of APP. Insofar as secreted APP has been proposed to have a neuroprotective function, the accumulation of A beta in the AD brain could decrease secreted APP and thereby indirectly increase A beta toxicity.

False

CitationGPTRetr11335

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta peptide induces cytochrome C release from isolated mitochondria. Abstract of the paper: Amyloid beta peptide (Abeta) is a neurotoxic metabolic product of the amyloid precursor protein (APP). Abeta is strongly implicated in the pathology of Alzheimer's disease (AD) and can be formed intracellularly. In this study, we show that the addition of Abeta to isolated mouse brain mitochondria can directly induce cytochrome c (Cyt c) release and mitochondrial swelling, which were partially inhibited by cyclosporin A (CsA). These results suggest that the Abetaaccumulated intracellularly by APP processing might exert neurotoxicity by interacting with mitochondria and inducing mitochondrial swelling and release of Cyt c, which activates caspase-3 and finally can lead to apoptosis in neuronal cells and to neurodegeneration in AD.

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CitationGPTRetr11336

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Multiple signaling events in amyloid beta-induced, oxidative stress-dependent neuronal apoptosis. Abstract of the paper: Current evidence suggests that amyloid beta peptides (Abeta) may play a major role in the pathogenesis of Alzheimer's disease by eliciting oxidative stress and neuronal apoptosis. In this study we have used differentiated SK-N-BE neurons to investigate molecular mechanisms and regulatory pathways underlying apoptotic neuronal cell death elicited by Abeta(1-40) and Abeta(1-42) peptides as well as the relationships between apoptosis and oxidative stress. Abeta peptides, used at concentrations able to induce oxidative stress, elicit a classic type of neuronal apoptosis involving mitochondrial regulatory proteins and pathways (i.e. affecting Bax and Bcl-2 protein levels as well as release of cytochrome c in the cytosol), poly-ADP rybose polymerase cleavage and activation of caspase 3. This pattern of neuronal apoptosis, that is significantly prevented by alpha-tocopherol and N-acetylcysteine and completely abolished by specific inhibitors of stress-activated protein kinases (SAPK) such as JNKs and p38(MAPK), involved early elevation of p53 protein levels. Pretreatment of neurons with alpha-pifithrin, a specific p53 inhibitor, resulted in a 50-60% prevention of Abeta induced apoptosis. These results suggest that oxidative stress - mediated neuronal apoptosis induced by amyloid beta operates by eliciting a SAPK-dependent multiple regulation of pro-apoptotic mitochondrial pathways involving both p53 and bcl-2.

False

CitationGPTRetr11337

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: beta-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease. Abstract of the paper: Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease. A major pathway of beta APP metabolism results in the release of secreted forms of beta APP, APPss. These secreted forms are released in response to electrical activity and can modulate neuronal responses to glutamate, suggesting roles in developmental and synaptic plasticity. beta APP is upregulated in response to neural injury and APPss can protect neurons against excitotoxic or ischemic insults by stabilizing the intracellular Ca2+ concentration [Ca2+]i. An alternative beta APP processing pathway liberates intact beta-amyloid peptide, which can form aggregates that disrupt Ca2+ homeostasis and render neurons vulnerable to metabolic or excitotoxic insults. Genetic abnormalities (e.g. certain beta APP mutations or Down syndrome) and age-related changes in brain metabolism (e.g. reduced energy availability or increased oxidative stress) may favor accumulation of [Ca2+]i-destabilizing beta-amyloid peptide and diminish the release of [Ca2+]i-stabilizing, neuroprotective APPss.

False

CitationGPTRetr11338

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Beta-amyloid peptides induce mitochondrial dysfunction and oxidative stress in astrocytes and death of neurons through activation of NADPH oxidase. Abstract of the paper: Beta-amyloid (betaA) peptide is strongly implicated in the neurodegeneration underlying Alzheimer's disease, but the mechanisms of neurotoxicity remain controversial. This study establishes a central role for oxidative stress by the activation of NADPH oxidase in astrocytes as the cause of betaA-induced neuronal death. betaA causes a loss of mitochondrial potential in astrocytes but not in neurons. The mitochondrial response consists of Ca2+-dependent transient depolarizations superimposed on a slow collapse of potential. The slow response is both prevented by antioxidants and, remarkably, reversed by provision of glutamate and other mitochondrial substrates to complexes I and II. These findings suggest that the depolarization reflects oxidative damage to metabolic pathways upstream of mitochondrial respiration. Inhibition of NADPH oxidase by diphenylene iodonium or 4-hydroxy-3-methoxy-acetophenone blocks betaA-induced reactive oxygen species generation, prevents the mitochondrial depolarization, prevents betaA-induced glutathione depletion in both neurons and astrocytes, and protects neurons from cell death, placing the astrocyte NADPH oxidase as a primary target of betaA-induced neurodegeneration.

False

CitationGPTRetr11339

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: previous studies demonstrated the direct effect of aβ peptides on mitochondrial motility Title of the paper: Amyloid beta peptide impaired carbachol but not glutamate-mediated phosphoinositide pathways in cultured rat cortical neurons. Abstract of the paper: Signal transduction systems, including cholinergic pathways, which are likely to be of pathophysiological significance are altered in Alzheimer's disease (AD). Muscarinic cholinergic receptors are linked to the hydrolysis of phosphoinositide, involving the production of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and the mobilization of cytosolic free calcium concentrations ([Ca2+]i). Effects of amyloid peptide (A(beta)) on these signals prior to neuronal degeneration were examined in cultured rat cortical cells. A(beta) increased the release of lactate dehydrogenase (LDH) in a concentration-dependent manner, however, it was blocked by B27 supplement. Prolonged exposure to a sublethal dose of A(beta) 25-35 or 1-42 disrupted carbachol-mediated release of Ins(1,4,5)P3 and [Ca2+]i, which was inhibited in media supplemented with B27 or the antioxidant vitamin E. In order to determine the specificity of the effect of A(beta), various agonists glutamate or KCl but not bradykinin which utilize the phosphoinositide cascade were investigated. Our results indicated that A(beta) did not affect the stimulation of glutamate or KCl-mediated production of Ins(1,4,5)P3 or cause elevation in [Ca2+]i. Furthermore, metabotropic agonist trans-1-amino-cyclopentane-1,3,-dicarboxylate (ACPD) elevated calcium level was not inhibited by A(beta) pre-treatment. Taken together, the results demonstrate that a sublethal dose of A(beta) selectively impaired cholinergic receptor-mediated signal transduction pathways, and antioxidant or B27 supplement attenuated this effect of A(beta). Alterations of cholinergic signaling by prolonged exposure to A(beta) could be involved in cortical neurodegeneration that occurs in AD. Because functional loss of cholinergic pathways is an important aspect of AD, the differences in susceptibility of these two types of receptors prior to other signs of A(beta) action is important and requires further investigation.

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CitationGPTRetr11340

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: A prospective study of dementia with Lewy bodies. Abstract of the paper: BACKGROUND little is known about the longitudinal course of dementia with Lewy bodies (DLB) and how this differs from Alzheimer's disease (AD). METHOD standardized baseline and annual assessments of cognitive and non-cognitive symptoms are reported in a cohort of 72 patients with DLB or AD. AD was diagnosed using the NINCDS ADRDA criteria and DLB was diagnosed with the criteria of McKeith et al. Cognitive assessment was undertaken using the MMSE schedule and operationalized definitions were used to diagnose non-cognitive symptoms. RESULTS 42 patients with DLB and 30 patients with AD were assessed. Of the 19 on whom post mortem examinations have been performed, 18 (95%) have had the clinical diagnosis confirmed. DLB patients were significantly more likely to experience visual hallucinations, disturbances of consciousness and parkinsonism at both baseline and at annual assessments. Of DLB patients exposed to neuroleptics, 33% developed sensitivity reactions. The magnitude and pattern of cognitive decline was similar in both groups. CONCLUSION the importance of the core features highlighted in the newly proposed consensus DLB criteria is supported. These features appear to be stable over time.

False

CitationGPTRetr11341

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Simple standardised neuropsychological assessments aid in the differential diagnosis of dementia with Lewy bodies from Alzheimer's disease and vascular dementia. Abstract of the paper: Consecutive patients from a dementia case register received a standardised evaluation which incorporated a neuropsychological assessment with the Cambridge Assessment for disorders in the elderly (CAMCOG). Operationalised clinical diagnoses were made (consensus criteria for dementia with Lewy bodies, DLB; NINCDS- ADRDA for Alzheimer's disease, AD, NINCDS AIRENS for vascular dementia, VaD). Two-hundred and twenty-eight patients were studied (DLB 54, AD102, VaD 72). DLB patients had significantly better performance on recent memory than AD patients, but more impaired visuospatial praxis. DLB patients also had significantly better recent memory than those with VaD. Optimal cut-off points for the recent memory:praxis ratio achieved good discrimination between DLB and both other dementias.

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CitationGPTRetr11342

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Research evaluation and prospective diagnosis of dementia with Lewy bodies. Abstract of the paper: OBJECTIVE To evaluate the relative merits of recently developed criteria for dementia with Lewy bodies (DLBs) in a longitudinal study of dementia. DESIGN The diagnosis of DLBs was used in combination with other clinical diagnosis. Patients were classified primarily based on the NINCDS-ADRDA (National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association) clinical criteria for probable or possible Alzheimer disease, or with other disease process that can cause dementia (eg, Parkinson disease), and secondarily according to the consensus guidelines for DLBs. This "double" clinical diagnosis was implemented to capture different pathological entities. The neuropathological diagnosis of Lewy bodies was made with monoclonal antibodies against alpha-synuclein. SETTING Multidisciplinary research clinic. RESULTS Prospective application of the consensus guidelines for DLBs from January 1, 1997, to September 29, 2000, identified 11 patients having the diagnosis of probable DLBs and 35 having possible DLBs. The diagnosis of probable or possible DLBs was associated with probable Alzheimer disease in 34 patients, with possible Alzheimer disease in 5 patients, with Parkinson disease in 2 patients, and with other disease processes in 2 patients. Three patients were diagnosed as having probable DLBs alone. An autopsy was performed in 26 of the cases who were clinically examined during the study period. Cortical Lewy bodies were identified in 13 cases; 4 had had premortem diagnosis of DLBs (sensitivity, 30.7%; specificity, 100%). CONCLUSIONS The prospective validation of the clinical criteria for DLBs showed poor accuracy in this series. We believe that current criteria for DLBs are useful when DLBs occur in isolation, but have low sensitivity when Lewy bodies coexist with the pathological abnormalities of Alzheimer disease.

False

CitationGPTRetr11343

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Accuracy of Clinical Diagnosis of Dementia with Lewy Bodies versus Neuropathology. Abstract of the paper: BACKGROUND The first consensus criteria for dementia with Lewy bodies (DLB) published in 1996 were revised in 2005, partly because the original clinical criteria had suboptimal sensitivity. Few studies have assessed the accuracy of the 2005 criteria applied prospectively in newly diagnosed patients who have been followed longitudinally. OBJECTIVE To explore the correlation between clinical and pathological diagnoses in patients with DLB and Parkinson's disease with dementia (PDD). METHODS From a prospective referral cohort study with enriched recruitment of patients with DLB and PDD, we included the first 56 patients coming to autopsy. Patients had mild dementia at inclusion and were followed annually until death with standardized clinical assessments. Pathological assessment was performed blind to clinical information according to standardized protocols and consensus criteria for DLB. RESULTS 20 patients received a pathological diagnosis of Lewy body disease; the corresponding clinical diagnoses were probable DLB (n = 11), PDD (n = 5), probable (n = 2) or possible (n = 2) Alzheimer's disease (AD). Of 14 patients with a clinical diagnosis of probable DLB, 11 had DLB/PDD and 3 had AD at pathology. One patient with clinically possible DLB fulfilled criteria for pathological AD. Sensitivity, specificity, positive predictive value, and negative predictive values for probable DLB were 73%, 93%, 79%, and 90%. CONCLUSION Our findings suggest that the international clinical consensus criteria for DLB perform reasonably well. However, false positive and false negative diagnoses still occur, indicating that the criteria need to be improved, that biomarkers may be needed, and that neuropathological feedback is vital to improve accuracy.

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CitationGPTRetr11344

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Dopamine transporter imaging for the diagnosis of dementia with Lewy bodies. Abstract of the paper: BACKGROUND Dementia with Lewy bodies (DLB) is a common cause of neurodegenerative dementia of old age. Its accurate recognition can be important in clinical management and is essential for the development of disease-modifying treatments. The current clinical diagnostic criteria are limited particularly by relatively poor sensitivity. Dopamine transporter (DAT) imaging using single-photon emission computed tomography (SPECT) is the most highly developed supplementary test for DLB, and is now incorporated as a suggestive feature in the consensus diagnostic criteria. However, there is uncertainty about its accuracy and its place in clinical practice. It is most commonly used in people who are already suspected of having DLB. OBJECTIVES We had two objectives in this review: (A) to estimate the accuracy of DAT imaging for the diagnosis of DLB in people with dementia in secondary care (specialist dementia services), and (B) to estimate the accuracy of DAT imaging for the diagnosis of DLB in people with dementia in secondary care who are already suspected of having DLB on the basis of a prior clinical work-up. SEARCH METHODS We searched MEDLINE (1946 to February 2013), Embase (1980 to February 2013), BIOSIS Previews (1926 to February 2013), PsycINFO (1806 to February 2013), CINAHL (1982 to February 2013), LILACS (February 2013) and Web of Science and Conference Proceedings (ISI Web of Science) (1945 to February 2013). Several of these sources contain conference abstracts. We also searched four specialised databases containing diagnostic reviews: Meta-analyses van Diagnostisch Onderzoek (MEDION; February 2013), Database of Abstracts of Reviews of Effects (DARE; February 2013), Health Technology Assessment Database (HTA; February 2013), and Aggressive Research Intelligence Facility (ARIF; February 2013). We checked reference lists of relevant studies and reviews for potential additional studies. Terms for electronic database searching were devised in conjunction with the team at the Cochrane Dementia and Cognitive Improvement Group. SELECTION CRITERIA STUDY DESIGN We included test accuracy studies with delayed verification, diagnostic case-control studies, and two-gate studies with alternative diagnosis controls. PARTICIPANTS (A) participants with dementia in secondary care, (B) participants in secondary care meeting consensus clinical criteria (other than the DAT imaging criterion) for possible or probable DLB, or both. INDEX TEST SPECT or positron emission tomography (PET) imaging of brain dopamine transporters. Reference standard: Neuropathological diagnosis at autopsy. DATA COLLECTION AND ANALYSIS Two review authors independently selected studies for inclusion and extracted data. We extracted results into a 2x2 table, showing the binary test results cross-classified with the binary reference standard. We used this data to calculate sensitivities, specificities, and their 95% confidence intervals. We used the QUADAS-2 tool plus some additional items to assess methodological quality. MAIN RESULTS We included one study that was applicable to our first objective (A). It reported data on 22 participants who met consensus clinical criteria for DLB or National Institute of Neurological and Communicative Disorders and Stroke and the Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) criteria for Alzheimer's disease, or both (a two-gate design with alternative diagnosis controls). The index test was SPECT scanning using the ligand (123)I-FP-CIT. We considered the study to be at high risk of bias in the participant selection and index test domains (QUADAS-2). (123)I-FP-CIT SPECT analysed semiquantitatively had a sensitivity of 1.00 (95% confidence interval (CI) 0.66 to 1.00) and a specificity of 0.92 (95% CI 0.64 to 1.00) for the diagnosis of DLB (n = 22, 1 study). Analysed visually, the sensitivity was 0.86 (95% CI 0.42 to 1.00) and the specificity was 0.83 (95% CI 0.52 to 0.98) (n = 19, 1 study).We considered that the study also provided the best available data to address our second objective (B). At baseline, 15 participants were clinically suspected of having DLB. In this group, (123)I-FP-CIT SPECT scanning analysed semiquantitatively had a sensitivity of 1.00 (95% CI 0.63 to 1.00) and a specificity of 1.00 (95% CI 0.59 to 1.00) for the diagnosis of DLB (n = 15, 1 study). Analysed visually, accuracy in this group was lower with a sensitivity of 0.83 (95% CI 0.36 to 1.00) and a specificity of 0.71 (95% CI 0.29 to 0.96) (n = 13, 1 study). AUTHORS' CONCLUSIONS Only one study has used a neuropathological reference standard to assess the accuracy of DAT imaging for the diagnosis of DLB. The small size of the included study means that sensitivity and specificity estimates are imprecise. However, data from this study suggest that DAT imaging is more accurate than clinical diagnosis. Clinical diagnosis is therefore unsuitable to use as a reference standard for assessing the accuracy of DAT imaging.No studies using a neuropathological reference standard have directly addressed the common clinical scenario where the use of DAT imaging is considered as a diagnostic test in a person with possible DLB, or assessed the accuracy of DAT imaging in people with mild dementia. However, the data from the included study suggest that, where there is moderately severe dementia and a strong pre-existing suspicion of DLB (probable DLB), then a normal (123)I-FP-CIT SPECT scan may be an accurate means of excluding the diagnosis.Semiquantitative ratings of (123)I-FP-CIT SPECT scans appeared to be more accurate than visual ratings in all analyses.

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CitationGPTRetr11345

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Validity of current clinical criteria for Alzheimer's disease, vascular dementia and dementia with Lewy bodies. Abstract of the paper: BACKGROUND Following the success of the NINCDS-ADRDA criteria for Alzheimer's disease, groups interested in vascular dementia and dementia with Lewy bodies have now adopted similar criteria. AIMS To assess whether the validity of these criteria are influenced by the prevalence of mixed pathologies or by the prevalence rate. METHOD A community based post-mortem study. RESULTS Mixed pathologies were common (33.8%). The high specificities obtained for the CDLB and NINDS-AIREN criteria (1.00 and 0.95, respectively) were associated with low sensitivities (0.22 and 0.43, respectively). Low prevalence and the presence of mixed pathologies had a deleterious effect on positive predictive values. CONCLUSIONS Current clinical diagnostic criteria are good at detecting pathology per se but not at detecting pure pathology. A large proportion of subjects from the general population fulfilling probable CDLB, probable NINCDS-ADRDA or probable NINDS-AIREN will have mixed pathologies.

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CitationGPTRetr11346

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Dementia with lewy bodies: findings from an international multicentre study. Abstract of the paper: OBJECTIVES To describe the baseline demographic, neuropsychiatric and neurological data of a large selected clinical sample of patients with dementia with Lewy Bodies (DLB) from an international multicentre trial with rivastigmine. To examine the usefulness of the Consensus Criteria for the diagnosis of DLB in different countries. METHODS Seventeen centres from Spain, the UK and Italy recruited patients diagnosed clinically as probable DLB according to recent Consensus Criteria (McKeith et al., 1996). A standard clinical protocol including inclusion/exclusion criteria, collection of demographic and medical data, cognitive (Mini Mental State Examination: MMSE), motor (Unified Parkinson's Disease Rating Scale: UPDRS) and neuropsychiatric (Neuropsychiatric Inventory: NPI) examinations, was applied after obtaining informed consent. Data were summarised and compared across countries with uni- and multivariate analyses. RESULTS One hundred and twenty patients were recruited: 56.7% males, mean (SD) age 73.9 (6.4) years, range 57 - 87 years. Sixty percent fulfilled all three core diagnostic features of DLB, and 40% only two ('parkinsonism' 92.4%, 'cognitive fluctuations' 89.1%, 'visual hallucinations' 77.3%). 'Systematised delusions' (46%) and 'repeated falls' (42%) were the most frequent supportive diagnostic features. There were no differences across countries in demographic, diagnostic or clinical features. Patients showed a wide range of psychopathology which was weakly correlated with cognitive impairment. Some mild extrapyramidal signs (EPS) were observed in most patients. CONCLUSIONS The Consensus Criteria for DLB can be consistently applied across many different sites for multicentre studies. 'Parkinsonism' and 'cognitive fluctuations' as core features and 'systematised delusions' and 'repeated falls' as supportive features are the most frequent diagnostic clues. Neuropsychiatric disturbances, in particular apathy, delusions, hallucinations and anxiety, and mild symmetric EPS are frequent in DLB and are only related weakly to cognitive impairment.

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CitationGPTRetr11347

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Clinical diagnosis of dementia. Abstract of the paper: This paper presents recommendations deriving from the Third Canadian Consensus Conference on the Diagnosis and Treatment of Dementia, concerning the clinical diagnosis of dementia. There are currently no universally accepted biological or radiological markers of dementia. In the absence of these, the diagnosis of dementia remains a clinical exercise aiming to integrate all available clinical and laboratory information. It is proposed that the currently used National Institute of Neurological and Communicative Disorders and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ADRA) criteria for diagnosis of Alzheimer's disease (AD) be retained. The currently available vascular dementia (VaD) diagnostic criteria have variable accuracy. An integrative approach to VaD diagnosis based on all the available evidence (history, vascular risk factors, physical exam, clinical course, neuroimaging, cognitive impairment pattern) is recommended. The separation of Lewy body dementia (DLB) from Parkinson's disease dementia (PDD) is based on the dominant clinical presenting feature of each syndrome, and relies on the duration of this feature: long duration of parkinsonian "motor" syndrome preceding dementia for PDD versus early/initial dementia accompanied by extrapyramidal symptoms for DLB. It is recognized that it is impossible clinically to characterize DLB with (pathologically) coexisting AD changes. The Frontotemporal group of dementia syndromes are discussed in regards to their typical clinical pictures, recognizing that their neuropathological substrate are not predictable from their mode of presentation. Finally, the particular rapid time sequence of evolution of the dementias due to prior disease is recognized as the clinically most useful distinguishing feature of these syndromes.

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CitationGPTRetr11348

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Long-Term Cognitive Decline in Dementia with Lewy Bodies in a Large Multicenter, International Cohort. Abstract of the paper: BACKGROUND/OBJECTIVE The aim of this study was to describe the rate and clinical predictors of cognitive decline in dementia with Lewy bodies (DLB), and compare the findings with Alzheimer's disease (AD) and Parkinson's disease dementia (PDD) patients. METHODS Longitudinal scores for the Mini-Mental State Examination (MMSE) in 1,290 patients (835 DLB, 198 PDD, and 257 AD) were available from 18 centers with up to three years longitudinal data. Linear mixed effects analyses with appropriate covariates were used to model MMSE decline over time. Several subgroup analyses were performed, defined by anti-dementia medication use, baseline MMSE score, and DLB core features. RESULTS The mean annual decline in MMSE score was 2.1 points in DLB, compared to 1.6 in AD (p = 0.07 compared to DLB) and 1.8 in PDD (p = 0.19). Rates of decline were significantly higher in DLB compared to AD and PDD when baseline MMSE score was included as a covariate, and when only those DLB patients with an abnormal dopamine transporter SPECT scan were included. Decline was not predicted by sex, baseline MMSE score, or presence of specific DLB core features. CONCLUSIONS The average annual decline in MMSE score in DLB is approximately two points. Although in the overall analyses there were no differences in the rate of decline between the three neurodegenerative disorders, there were indications of a more rapid decline in DLB than in AD and PDD. Further studies are needed to understand the predictors and mechanisms of cognitive decline in DLB.

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CitationGPTRetr11349

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Evaluation of the NINCDS-ADRDA criteria in the differentiation of Alzheimer's disease and frontotemporal dementia. Abstract of the paper: OBJECTIVES The diagnosis of Alzheimer's disease (AD) is now reliant on the use of NINCDS-ADRDA criteria. Other diseases causing dementia are being increasingly recognised--for example, frontotemporal dementia (FTD). Historically, these disorders have not been clearly demarcated from AD. This study assesses the capability of the NINCDS-ADRDA criteria to accurately distinguish AD from FTD in a series of pathologically proved cases. METHODS The case records of 56 patients (30 with AD, 26 with FTD) who had undergone neuropsychological evaluation, brain imaging, and ultimately postmortem, were assessed in terms of whether at initial diagnosis the NINCDS-ADRDA criteria were successful in diagnosing those patients who had AD and excluding those who did not. RESULTS (1) The overall sensitivity of the NINCDS-ADRDA criteria in diagnosing "probable" AD from 56 patients with cortical dementia (AD and FTD) was 0.93. However, the specificity was only 0.23; most patients with FTD also fulfilled NINCDS-ADRDA criteria for AD. (2) Cognitive deficits in the realms of orientation and praxis significantly increased the odds of a patient having AD compared with FTD, whereas deficits in problem solving significantly decreased the odds. Neuropsychological impairments in the domains of attention, language, perception, and memory as defined in the NINCDS-ADRDA statement did not contribute to the clinical differentiation of AD and FTD. CONCLUSION NINCDS-ADRDA criteria fail accurately to differentiate AD from FTD. Suggestions to improve the diagnostic specificity of the current criteria are made.

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CitationGPTRetr11350

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Accurate prediction of histologically confirmed Alzheimer's disease and the differential diagnosis of dementia: the use of NINCDS-ADRDA and DSM-III-R criteria, SPECT, X-ray CT, and Apo E4 in medial temporal lobe dementias. Oxford Project to Investigate Memory and Aging. Abstract of the paper: In a prospective study of more than 200 cases of dementia and 119 controls, annual technetium-99m-hexamethyl-propylene amineoxime (99mTC-HMPAO) single-photon emission computed tomography (SPECT) and annual medial temporal lobe (MTL) oriented X-ray computed tomography (CT) have been used to evaluate the diagnostic potential of functional and structural neuroimaging in the differential diagnosis of dementia. Some subjects have had up to 7 annual evaluations. So far, of 151 who have died, 143 (95%) have come to necropsy. Histology is known for 118, of whom 80 had Alzheimer's disease (AD), 24 had other "non-AD" dementias, and 14 controls with no cognitive deficit in life also had no significant central nervous system pathology. To compare the findings in the dementias with the profile of structural and functional imaging in the cognitively normal elderly, scan data from 105 living, elderly controls without cognitive deficit have also been included in the analysis. All clinical diagnoses were according to National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS-ADRDA) and the Diagnostic and Statistical Manual of Mental Disorders (3rd ed., rev.; DSM-III-R) criteria, and all histopathological diagnoses according to the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria. Early data from this cohort have suggested that the combination of both MTL atrophy seen on CT with parietotemporal hypoperfusion on SPECT may predict the pathology of AD. The diagnostic sensitivity, specificity, accuracy, and positive and negative predictive values of the NINCDS-ADRDA and DSM-III-R criteria could be assessed in this cohort against the gold standard of histopathology. The diagnostic potential of CT evidence of MTL atrophy alone, SPECT evidence of parietotemporal hypoperfusion alone, and the combination of both of these scan changes in the same individual could then be compared against the diagnostic accuracy of clinical operational criteria in the pathologically confirmed cases. Furthermore, all of these modalities could be compared with the diagnostic accuracy of apolipoprotein E4 (Apo E4) genotyping to predict AD in the histopathologically confirmed cohort. In this population, NINCDS "probable-AD" was 100% specific, 49% sensitive, and 66% accurate; "possible-AD" was only 61% specific, but 93% sensitive and 77% accurate; and the combination of both "probable-AD" and "possible-AD" was 61% specific, 96% sensitive, and 85% accurate. DSM-III-R criteria were 51% sensitive, 97% specific, and 66% accurate. In the same cases and including the 105 living, elderly controls, the diagnostic accuracy of the Oxford Project to Investigate Memory and Aging (OPTIMA) scanning criteria showed CT alone to be 85% sensitive, 78% specific, and 80% accurate; SPECT alone had 89% sensitivity, 80% specificity, and 83% accuracy; and the combination of the two was 80% sensitive, 93% specific, and 88% accurate. The Apo E4 genotype was 74% sensitive but yielded 40% false positives in the histologically confirmed series. The diagnostic accuracy afforded by this method of CT and SPECT used alone is better than that of any established clinical criteria and reveals that the combination of MTL atrophy and parietotemporal hypoperfusion is common in AD, much less common in other dementias, and rare in normal controls. In the NINCDS-ADRDA criteria "possible-AD" cases, the combination of CT and SPECT findings alone were better in all diagnostic indices than the presence of Apo E4 alone in predicting AD. The frequent occurrence of MTL atrophy in AD and also in other "non-AD" dementias later in the course of the disease suggests the concept of medial temporal lobe dementia. This could explain some of the overlap of clinical profiles in the dementias, particularly as the dementia progresses, making clinical differential diagnosis difficult. In this context, the use of SPECT can significantl

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CitationGPTRetr11351

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Clinical Lewy body dementia and the impact of vascular components. Abstract of the paper: OBJECTIVE To study the prevalence of patients fulfilling the clinical consensus criteria for dementia with Lewy bodies (DLB) in a dementia population followed up with postmortem examination. To compare the clinical and neuropathological findings in the clinical Lewy body dementia (LBD) group with findings in a clinically defined group with Alzheimer's disease (AD). DESIGN Medical records from 200 patients were studied retrospectively. Clinical consensus criteria for DLB and clinical criteria for other dementias were applied. SETTING The majority of the cases were examined and cared for in psychogeriatric and psychiatric departments. PATIENTS The patients, who died between 1985 and 1994, were part of a longitudinal dementia project. Each case was neuropathologically examined. Main outcome measures Prevalence of clinical signs and neuropathology was compared between the clinical groups. RESULTS Forty-eight (24%) patients fulfilled the clinical criteria for DLB while 45 (22%) fulfilled the clinical criteria for Alzheimer's disease. The clinical LBD group had a higher Hachinski score compared to the clinical AD group. They also showed a tendency towards a 'frontal profile' with disinhibition, confusion, personality change and vocally disruptive behaviour. More than 80% of the AD and LBD groups respectively exhibited Alzheimer pathology. The LBD group had frontal white matter pathology and degeneration of the substantia nigra more often than the clinical AD group. Both LBD and AD groups showed a progressive and marked increase in severity of dementia and decrease in ADL capacity according to an evaluation based on the Berger scale and Katz index. The condition of the LBD group was significantly worse earlier in dementia. CONCLUSION The results of this study indicate that patients fulfilling the clinical criteria for DLB also exhibit clinical features of possible vascular origin and a frontal profile. Subcortical vascular pathology, nigral degeneration and AD pathology in this group could partly explain the clinical features used to define DLB.

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CitationGPTRetr11352

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Clinicopathological analysis of dementia disorders in the elderly. Abstract of the paper: The relative incidence of the major types of dementia disorders and the agreement rates between clinical and pathological diagnosis were analysed in consecutive autopsy series of 675 demented subjects from 3 hospitals (mean age 79.5 years, SD 9.6). Clinical assessment followed the DSM-III and ICD-9-NA criteria and NINCDS/ADRDA criteria for probable Alzheimer disease (AD) (McKhann et al. 1984), histological criteria for the diagnosis of AD those of the NIH/AARP Work Group (Khachaturian 1985) using a 4-degree rating scale for plaques and tangles in neocortex and hippocampus (Morris et al. 1988), and the criteria by Tierney et al. (1988) for 'pure' AD. Vascular dementia (MID) and other disorders were diagnosed according to current pathologic criteria. Clinical diagnosis of AD/SDAT was made in 59.2%, of MID in 21.7%, of mixed AD + MID in 3.1%, and of Parkinson's disease (PD) and other disorders in 16%. At autopsy, 76.7% fulfilled histological criteria for AD/SDAT, but only 60% were 'pure' forms, while 8.2% had additional features of PD and 7.9% coexisting vascular lesions indicating mixed SDAT + MID. 15.7% were MID with no or very little AD pathology, 7.4% other CNS disorders. 0.3% of the brains showed no abnormality beyond age-related changes. AD/SDAT had its highest incidence in a psychiatric population, MID and PD + SDAT in general and geriatric hospital cohorts. The overall coincidence rates for clinical and pathological diagnosis of AD/SDAT were 85.2%, for MIX and MID 60.5-61.9%, but only 51% for PD-PD/AD. These data and the results of other recent studies emphasize the need for more appropriate clinical and pathological criteria in the diagnosis of the dementias.

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CitationGPTRetr11353

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Performance on the dementia rating scale in Parkinson's disease with dementia and dementia with Lewy bodies: comparison with progressive supranuclear palsy and Alzheimer's disease. Abstract of the paper: BACKGROUND The relation between dementia with Lewy bodies (DLB) and Parkinson's disease with dementia (PDD) is unknown. OBJECTIVES To compare the cognitive profiles of patients with DLB and PDD, and compare those with the performance of patients with a subcortical dementia (progressive supranuclear palsy) and a cortical dementia (Alzheimer's disease). DESIGN Survey of cognitive features. SETTING General community in Rogaland county, Norway, and a university dementia and movement disorder research centre in the USA. PATIENTS 60 patients with DLB, 35 with PDD, 49 with progressive supranuclear palsy, and 29 with Alzheimer's disease, diagnosed by either standardised clinical procedures and criteria (all PDD and Alzheimer cases and 76% of cases of progressive supranuclear palsy), or necropsy (all DLB cases and 24% of cases of progressive supranuclear palsy). Level of dementia severity was matched using the total score on the dementia rating scale adjusted for age and education. MAIN OUTCOME MEASURES Dementia rating scale subscores corrected for age. RESULTS No significant differences between the dementia rating scale subscores in the PDD and DLB groups were found in the severely demented patients; in patients with mild to moderate dementia the conceptualisation subscore was higher in PDD than in DLB (p = 0.03). Compared with Alzheimer's disease, PDD and DLB had higher memory subscores (p < 0.001) but lower initiation and perseveration (p = 0.008 and p=0.021) and construction subscores (p = 0.009 and p = 0.001). DLB patients had a lower conceptualisation subscore (p = 0.004). Compared with progressive supranuclear palsy, PDD and DLB patients had lower memory subscores (p < 0.001). CONCLUSIONS The cognitive profiles of patients with DLB and PDD were similar, but they differed from those of patients with Alzheimer's disease and progressive supranuclear palsy. The cognitive pattern in DLB and PDD probably reflects the superimposition of subcortical deficits upon deficits typically associated with Alzheimer's disease.

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CitationGPTRetr11354

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Dementia with Lewy bodies: a comparison of clinical diagnosis, FP-CIT single photon emission computed tomography imaging and autopsy. Abstract of the paper: BACKGROUND Dementia with Lewy bodies (DLB) is a common form of dementia. The presence of Alzheimer's disease (AD) pathology modifies the clinical features of DLB, making it harder to distinguish DLB from AD clinically during life. Clinical diagnostic criteria for DLB applied at presentation can fail to identify up to 50% of cases. Our aim was to determine, in a series of patients with dementia in whom autopsy confirmation of diagnosis was available, whether functional imaging of the nigrostriatal pathway improves the accuracy of diagnosis compared with diagnosis by means of clinical criteria alone. METHODS A single photon emission computed tomography (SPECT) scan was carried out with a dopaminergic presynaptic ligand [123I]-2beta-carbometoxy-3beta-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (FP-CIT; ioflupane) on a group of patients with a clinical diagnosis of DLB or other dementia. An abnormal scan was defined as one in which right and left posterior putamen binding, measured semiquantitatively, was more than 2 SDs below the mean of the controls. RESULTS Over a 10 year period it was possible to collect 20 patients who had been followed from the time of first assessment and time of scan through to death and subsequent detailed neuropathological autopsy. Eight patients fulfilled neuropathological diagnostic criteria for DLB. Nine patients had AD, mostly with coexisting cerebrovascular disease. Three patients had other diagnoses. The sensitivity of an initial clinical diagnosis of DLB was 75% and specificity was 42%. The sensitivity of the FP-CIT scan for the diagnosis of DLB was 88% and specificity was 100%. CONCLUSION FP-CIT SPECT scans substantially enhanced the accuracy of diagnosis of DLB by comparison with clinical criteria alone.

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CitationGPTRetr11355

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Diagnostic Criteria for Dementia with Lewy Bodies: Updates and Future Directions. Abstract of the paper: The aim of this article is to describe the 2017 revised consensus criteria for the clinical diagnosis of dementia with Lewy bodies (DLB) with future directions for the diagnostic criteria. The criteria for the clinical diagnosis of probable and possible DLB were first published as the first consensus report in 1996 and were revised in the third consensus report in 2005. After discussion at the International DLB Conference in Fort Lauderdale, Florida, USA, in 2015, the International DLB Consortium published the fourth consensus report including the revised consensus criteria in 2017. The 2017 revised criteria clearly distinguish between clinical features and diagnostic biomarkers. Significant new information about previously reported aspects of DLB has been incorporated, with increased diagnostic weighting given to rapid eye movement (REM) sleep behavior disorder (RBD) and iodine-123-metaiodobenzylguanidine (MIBG) myocardial scintigraphy. Future directions include the development of the criteria for early diagnosis (prodromal DLB) and the establishment of new biomarkers that directly indicate Lewy-related pathology, including α-synuclein imaging, biopsies of peripheral tissues (skin, etc.) for the demonstration of α-synuclein deposition, and biochemical markers (cerebrospinal fluid/blood), as well as the pathological evaluation of the sensitivity and specificity of the 2017 revised diagnostic criteria. In conclusion, the revised consensus criteria for the clinical diagnosis of DLB were reported with the incorporation of new information about DLB in 2017. Future directions include the development of the criteria for early diagnosis and the establishment of biomarkers directly indicative of Lewy-related pathology.

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CitationGPTRetr11356

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: A 6-year study of cognition and spatial function in the demented and non-demented elderly: the Sydney Older Persons Study. Abstract of the paper: BACKGROUND Spatial function has been suggested to be disproportionately worse in people with dementia with Lewy bodies (DLB) than other dementia groups, and poor performance on the Mini-Mental State Examination pentagon copying (PC) task has been proposed as adequate for assessing this. We aimed to establish the prevalence of poor PC in the non-demented elderly; determine the validity of the use of PC as a spatial function test, and determine if poor PC is more common in DLB than non-DLB dementias. METHODS In a population-based sample of 299 participants, 126 were rated as being cognitively normal (clinical rating scale [CDR] = 0), 95 mildly cognitively impaired (CDR = 0.5), and 78 met criteria for dementia, 19 of whom met criteria for probable DLB (pDLB) and 25 with none of the core features of DLB (non-DLB). The accuracy of PC performance was determined across CDR groups, and the relationship of PC to performance on a broad range of cognitive tests was evaluated. The dementia groups were compared cross-sectionally to determine differences in PC and other cognitive test performance, as well as 3 and 6 years earlier to determine cognitive differences at initial stages of cognitive decline. RESULTS Poor PC was common in the non-demented elderly (39% CDR = 0; 43% CDR = 0.5). In this non-demented group, PC was selectively related to tests of spatial function. Poor PC was not significantly different in the pDLB and non-DLB groups at any assessment time, however it became more prevalent as dementia severity increased. Memory function and verbal fluency were more impaired in the pDLB group in the early stages of the disorder. COMMENT PC appears to be a good measure of spatial function in the elderly. However, in contrast to other findings of poor spatial skills in DLB when dementia is in the mild to moderate stages, poor PC performance has not been shown to be a good early marker of DLB and its clinical correlates are yet to be determined.

False

CitationGPTRetr11357

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Neuroimaging characteristics of dementia with Lewy bodies. Abstract of the paper: This review summarises the findings and applications from neuroimaging studies in dementia with Lewy bodies (DLB), highlighting key differences between DLB and other subtypes of dementia. We also discuss the increasingly important role of imaging biomarkers in differential diagnosis and outline promising areas for future research in DLB. DLB shares common clinical, neuropsychological and pathological features with Parkinson's disease dementia and other dementia subtypes, such as Alzheimer's disease. Despite the development of consensus diagnostic criteria, the sensitivity for differential diagnosis of DLB in clinical practice remains low and many DLB patients will be misdiagnosed. The importance of developing accurate imaging markers in dementia is highlighted by the potential for treatments targeting specific molecular abnormalities as well as the responsiveness to cholinesterase inhibitors and marked neuroleptic sensitivity of DLB. We review various brain imaging techniques that have been applied to investigate DLB, including the characteristic nigrostriatal degeneration in DLB using positron emission tomography (PET) and single-photon emission computed tomography (SPECT) tracers. Dopamine transporter loss has proven to reliably differentiate DLB from other dementias and has been incorporated into the revised clinical diagnostic criteria for DLB. To date, this remains the 'gold standard' for diagnostic imaging of DLB. Regional cerebral blood flow, 18 F-fluorodeoxygluclose-PET and SPECT have also identified marked deficits in the occipital regions with relative sparing of the medial temporal lobe when compared to Alzheimer's disease. In addition, structural, diffusion, and functional magnetic resonance imaging techniques have shown alterations in structure, white matter integrity, and functional activity in DLB. We argue that the multimodal identification of DLB-specific biomarkers has the potential to improve ante-mortem diagnosis and contribute to our understanding of the pathological background of DLB and its progression.

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CitationGPTRetr11358

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: Prospective validation of consensus criteria for the diagnosis of dementia with Lewy bodies. Abstract of the paper: OBJECTIVE To determine the validity of a clinical diagnosis of probable or possible dementia with Lewy bodies (DLB) made using International Consensus criteria. BACKGROUND Validation studies based on retrospective chart reviews of autopsy-confirmed cases have suggested that diagnostic specificity for DLB is acceptable but case detection rates as low as 0.22 have been suggested. METHODS We evaluated the first 50 cases reaching neuropathologic autopsy in a cohort to which Consensus clinical diagnostic criteria for DLB, National Institute for Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for AD, and National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et l'Enseignement en Neurosciences criteria for vascular dementia (VaD) had been prospectively applied. RESULTS Twenty-six clinical diagnoses of DLB, 19 of AD, and 5 of VaD were made. At autopsy, 29 DLB cases, 15 AD, 5 VaD, and 1 progressive supranuclear palsy were identified. The sensitivity and specificity of a clinical diagnosis of probable DLB in this sample were 0.83 and 0.95. Of the five cases receiving a false-negative diagnosis of DLB, significant fluctuation was present in four but visual hallucinations and spontaneous motor features of parkinsonism were generally absent. Thirty-one percent of the DLB cases had additional vascular pathology and in two cases this contributed to a misdiagnosis of VaD. No correlations were found between the distribution of Lewy bodies and clinical features. CONCLUSION The Consensus criteria for DLB performed as well in this prospective study as those for AD and VaD, with a diagnostic sensitivity substantially higher than that reported by previous retrospective studies. DLB occurs in the absence of extrapyramidal features and in the presence of comorbid cerebrovascular disease. Fluctuation is an important diagnostic indicator, reliable measures of which need to be developed further.

False

CitationGPTRetr11359

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: data were collected as part of a phase 3 multicentre imaging study whose methodology is described in detail elsewhere in brief patients were aged 5590 years and met the criteria for dementia detailed in dsmiv and fulfilled at least one of the following consensus criteria for dlb nincdsadrda criteria for probable or possible ad or nindsairen criteria for probable or possible vascular dementia a minimental state examination mmse score at baseline of 10 was required to ensure patients could complete assessments patients with dementia who developed parkinsonism 1 year before the onset of dementia were deemed to have parkinsons disease with dementia and were not included those with structural imaging findings indicative of infarction in the region of the basal ganglia including the internal capsule were excluded Title of the paper: [Dementia with Lewy bodies and Alzheimer's disease: differential diagnosis by cardiac sympathetic innervation MIBG imaging]. Abstract of the paper: UNLABELLED Dementia with Lewy bodies (DLB) is the second most common cause of degenerative dementia after Alzheimer's disease (AD). At present, pre-mortem diagnosis of DLB can only be made clinically using the International Consensus Criteria. However, an accurate differential diagnosis between these diseases could improve the therapeutic handling of patients with DLB, due to their supersensitivity to neuroleptic treatment and the difficult treatment of their psychotic symptoms. OBJECTIVE To assess the utility of cardiac MIBG imaging as diagnostic study for DLB, to help in the differential diagnosis with AD. MATERIAL AND METHODS Cardiac MIBG imaging was performed in 11 patients with clinical criteria of probable DLB (7 males, mean age 77 years [range 62-89 years], mean MMSE 17 [range 11-28], and in 9 patients with clinical criteria of probable AD (3 males, mean age 79 years [range 61-87 years], mean MMSE 17 [range 4-25]). Planar anterior images of the thorax were acquired at 15 minutes. (early study) and 4 hours (late study) after tracer injection. Myocardial MIBG activity was quantified by means of a heart-to-mediastinum ratio (HMR). A HMR > 1.8 was considered normal. RESULTS Respect AD patients, patients with DLB showed decreased HMR in the early study (1.34 +/- 0.27 [range 1.03-1.98] vs. 1.84 +/- 0.22 [range 1.53-2.15], p<0.001) and in the late study (1.22 +/- 0.23 [range 0.95-1.75] vs. 1.73 +/- 0.08 [range 1.59-1.89], p<0.0001). CONCLUSIONS Cardiac MIBG imaging could be a useful tool for differential diagnosis between DLB and AD.

False

CitationGPTRetr11360

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Oxidative stress in Alzheimer's disease brain: new insights from redox proteomics. Abstract of the paper: Alzheimer's disease, an age-related neurodegenerative disorder, is characterized clinically by a progressive loss of memory and cognitive functions. Neuropathologically, Alzheimer's disease is defined by the accumulation of extracellular amyloid protein deposited senile plaques and intracellular neurofibrillary tangles made of abnormal and hyperphosphorylated tau protein, regionalized neuronal death, and loss of synaptic connections within selective brain regions. Evidence has suggested a critical role for amyloid-beta peptide metabolism and oxidative stress in Alzheimer's disease pathogenesis and progression. Among the other indices of oxidative stress in Alzheimer's disease brain are protein carbonyls and 3-nitrotyrosine, which are the markers of protein oxidation. Thus, in this review, we discuss the application of redox proteomics for the identification of oxidatively modified proteins in Alzheimer's disease brain and also discuss the functions associated with the identified oxidized proteins in relation to Alzheimer's disease pathology. The information obtained from proteomics may be helpful in understanding the molecular mechanisms involved in the development and progression of Alzheimer's disease as well as of other neurodegenerative disorders. Further, redox proteomics may provide potential targets for drug therapy in Alzheimer's disease.

False

CitationGPTRetr11361

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairment. Abstract of the paper: Oxidative damage is a feature of many age-related neurodegenerative diseases, including Alzheimer's disease (AD). 4-Hydroxy-2-nonenal (HNE) is a highly reactive product of the free radical-mediated lipid peroxidation of unsaturated lipids, particularly arachidonic acid, in cellular membranes. In the present study we show for the first time in brain obtained at short postmortem intervals that the levels of HNE are elevated in mild cognitive impairment (MCI) hippocampus and inferior parietal lobules compared to those of control brain. Thus, increased levels of HNE in MCI brain implicate lipid peroxidation as an early event in AD pathophysiology and also suggest that the pharmacologic intervention to prevent lipid peroxidation at the MCI stage or earlier may be a promising therapeutic strategy to delay or prevent progression to AD.

False

CitationGPTRetr11362

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Redox proteomics identification of 4-hydroxynonenal-modified brain proteins in Alzheimer's disease: Role of lipid peroxidation in Alzheimer's disease pathogenesis. Abstract of the paper: Numerous studies have shown that neuronal lipids are highly susceptible to oxidative stress including in those brain areas directly involved in the neurodegenerative process of Alzheimer's disease (AD). Lipid peroxidation directly damages membranes and also generates a number of secondary biologically active products (toxic aldehydes)that are capable of easily attacking lipids, proteins, and DNA. Accumulating evidence has demonstrated regionally increased brain lipid peroxidation in patients with AD; however, extensive studies on specific targets of lipid peroxidation-induced damage are still missing. The present study represents a further step in understanding the relationship between oxidative modification of protein and neuronal death associated with AD. We used a proteomics approach to determine specific targets of lipid peroxidation in AD brain, both in hippocampus and inferior parietal lobule, by coupling immunochemical detection of 4-hydroxynonenal-bound proteins with 2-D polyacrylamide gel electrophoresis and MS analysis. We identified 4-hydroxynonenal-bound proteins in the hippocampus and inferior parietal lobule brain regions of subjects with AD. The identified proteins play different biological functions including energy metabolism, antioxidant system, and structural proteins, thus impairing multiple molecular pathways. Our results provide further evidence for the role of lipid peroxidation in the pathogenesis of AD.

False

CitationGPTRetr11363

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Four-hydroxynonenal, a product of lipid peroxidation, is increased in the brain in Alzheimer's disease. Abstract of the paper: Recent studies have implicated increased oxidative stress in the pathogenesis of Alzheimer's disease (AD). Increased lipid peroxidation and decreased polyunsaturated fatty acid levels have been described in the brain in AD. Four-hydroxynonenal (HNE), an aldehyde product of lipid peroxidation, has been demonstrated to be a neurotoxin in tissue culture and in vivo studies and is elevated in ventricular fluid in AD. We report here an increase in mean free HNE in multiple brain regions in AD compared with age-matched control subjects. These increases reached statistical significance in the amygdala and hippocampus and parahippocampal gyrus, regions showing the most pronounced histopathological alterations in AD. This study, in conjunction with cell culture studies, suggests that HNE may be an important substance in the pathogenesis of neuron degeneration in AD.

True

CitationGPTRetr11364

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer's disease. Abstract of the paper: Alzheimer's disease (AD) is an age-related neurodegenerative disorder. A number of hypotheses have been proposed to explain AD pathogenesis. One such hypothesis proposed to explain AD pathogenesis is the oxidative stress hypothesis. Increased levels of oxidative stress markers including the markers of lipid peroxidation such as acrolein, 4-hydroxy-2-trans-nonenal (HNE), malondialdehyde, etc. are found in brains of AD subjects. In this review, we focus principally on research conducted in the area of HNE in the central nervous system (CNS) of AD and mild cognitive impairment (MCI), and further, we discuss likely consequences of lipid peroxidation with respect to AD pathogenesis and progression. Based on the research conducted so far in the area of lipid peroxidation, it is suggested that lipid accessible antioxidant molecules could be a promising therapeutic approach to treat or slow progression of MCI and AD.

False

CitationGPTRetr11365

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Role of 4-hydroxy-2-nonenal (HNE) in the pathogenesis of alzheimer disease and other selected age-related neurodegenerative disorders. Abstract of the paper: Oxidative stress is involved in various and numerous pathological states including several age-related neurodegenerative diseases. Peroxidation of the membrane lipid bilayer is one of the major sources of free radical-mediated injury that directly damages neurons causing increased membrane rigidity, decreased activity of membrane-bound enzymes, impairment of membrane receptors and altered membrane permeability and eventual cell death. Moreover, the peroxidation of polyunsaturated fatty acids leads to the formation of aldehydes, which can act as toxic by-products. One of the most abundant and cytotoxic lipid -derived aldehydes is 4-hydroxy 2-nonenal (HNE). HNE toxicity is mainly due to the alterations of cell functions by the formation of covalent adducts of HNE with proteins. A key marker of lipid peroxidation, HNE-protein adducts, were found to be elevated in brain tissues and body fluids of Alzheimer disease, Parkinson disease, Huntington disease and amyotrophic lateral sclerosis subjects and/or models of the respective age-related neurodegenerative diseases. Although only a few proteins were identified as common targets of HNE modification across all these listed disorders, a high overlap of these proteins occurs concerning the alteration of common pathways, such as glucose metabolism or mitochondrial function that are known to contribute to cognitive decline. Within this context, despite the different etiological and pathological mechanisms that lead to the onset of different neurodegenerative diseases, the formation of HNE-protein adducts might represent the shared leit-motif, which aggravates brain damage contributing to disease specific clinical presentation and decline in cognitive performance observed in each case.

False

CitationGPTRetr11366

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Redox proteomic identification of 4-hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer's disease. Abstract of the paper: Numerous investigations point to the importance of oxidative imbalance in mediating AD pathogenesis. Accumulated evidence indicates that lipid peroxidation is an early event during the evolution of the disease and occurs in patients with mild cognitive impairment (MCI). Because MCI represents a condition of increased risk for Alzheimer's disease (AD), early detection of disease markers is under investigation. Previously we showed that HNE-modified proteins, markers of lipid peroxidation, are elevated in MCI hippocampus and inferior parietal lobule compared to controls. Using a redox proteomic approach, we now report the identity of 11 HNE-modified proteins that had significantly elevated HNE levels in MCI patients compared with controls that span both brain regions: Neuropolypeptide h3, carbonyl reductase (NADPH), alpha-enolase, lactate dehydrogenase B, phosphoglycerate kinase, heat shock protein 70, ATP synthase alpha chain, pyruvate kinase, actin, elongation factor Tu, and translation initiation factor alpha. The enzyme activities of lactate dehydrogenase, ATP synthase, and pyruvate kinase were decreased in MCI subjects compared with controls, suggesting a direct correlation between oxidative damage and impaired enzyme activity. We suggest that impairment of target proteins through the production of HNE adducts leads to protein dysfunction and eventually neuronal death, thus contributing to the biological events that may lead MCI patients to progress to AD.

False

CitationGPTRetr11367

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Increased oxidative stress in Alzheimer's disease as assessed with 4-hydroxynonenal but not malondialdehyde. Abstract of the paper: Oxidative stress is thought to play a major role in the pathogenesis of Alzheimer's disease (AD). Although there is strong post-mortem and experimental evidence of oxidative damage occurring in AD brains, the use of markers in the peripheral circulation to show oxidative stress is less convincing. We examined plasma from AD patients for markers of increased oxidative stress. We report elevated levels of 4-hydroxy-nonenal (4-HNE) in AD patients compared to controls (median 20.6, IQR 6.0-25.2 vs. 7.8, 3.3-14.5 micomol/l, respectively; p=0.001) but not malondialdehyde (MDA), and lower levels of ascorbate in AD plasma when compared to age-matched controls (9.9, 6.0-33.7 vs. 24.2, 13.9-48.6 micromol/l; p<0.05). Levels of 4-HNE in AD patients were inversely related to ascorbate (r=-0.337; p=0.07) and Folstein Mini-Mental State Examination (MMSE) (r=-0.474; p=0.015). The concentration of protein sulphydryls, free-radical scavengers, was directly related to the MMSE result (r=0.427; p=0.03). Increased production of 4-HNE indicates increased oxidative stress (lipid peroxidation), which is not evident using the more common marker MDA. This elevation of 4-HNE was related to the degree of cognitive impairment (MMSE).

False

CitationGPTRetr11368

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: 4-Hydroxy-2-nonenal: a product and mediator of oxidative stress. Abstract of the paper: The onset of lipid peroxidation within cellular membranes is associated with changes in their physiochemical properties and with the impairment of enzymatic functions located in the membrane environment. There is increasing evidence that aldehydic molecules generated endogenously during the process of lipid peroidation are causally involved in most of the pathophysiological effects associated with oxidative stress in cells and tissues. 4-Hydroxy-2-nonenal (HNE), among them, is believed to be largely responsible for cytopathological effects observed during oxidative stree in vivo and has achieved the status of one of the best recognized and most studied of the cytotoxic products of lipid peroxidation. In the present review, I provide a comprehensive summary of HNE, as the product and mediator or oxidative stress.

True

CitationGPTRetr11369

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: 4-Hydroxynonenal (HNE) modified proteins in metabolic diseases. Abstract of the paper: 4-Hydroxynonenal (HNE) is one of the quantitatively most important products of lipid peroxidation. Due to its high toxicity it is quickly metabolized, however, a small share of HNE avoids enzymatic detoxification and reacts with biomolecules including proteins. The formation of HNE-protein-adducts is one of the accompanying processes in oxidative stress or redox disbalance. The modification of proteins might occur at several amino acids side chains, leading to a variety of products and having effects on the protein function and fate. This review summarizes current knowledge on the formation of HNE-modified proteins, their fate in mammalian cells and their potential role as a damaging agents during oxidative stress. Furthermore, the potential of HNE-modified proteins as biomarkers for several diseases are highlighted.

False

CitationGPTRetr11370

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: A Review of Oxidative Stress Products and Related Genes in Early Alzheimer's Disease. Abstract of the paper: Oxidative stress is associated with the progression of Alzheimer's disease (AD). Reactive oxygen species can modify lipids, DNA, RNA, and proteins in the brain. The products of their peroxidation and oxidation are readily detectable at incipient stages of disease. Based on these oxidation products, various biomarker-based strategies have been developed to identify oxidative stress levels in AD. Known oxidative stress-related biomarkers include lipid peroxidation products F2-isoprostanes, as well as malondialdehyde and 4-hydroxynonenal which both conjugate to specific amino acids to modify proteins, and DNA or RNA oxidation products 8-hydroxy-2'-deoxyguanosine (8-OHdG) and 8-hydroxyguanosine (8-OHG), respectively. The inducible enzyme heme oxygenase type 1 (HO-1) is found to be upregulated in response to oxidative stress-related events in the AD brain. While these global biomarkers for oxidative stress are associated with early-stage AD, they generally poorly differentiate from other neurodegenerative disorders that also coincide with oxidative stress. Redox proteomics approaches provided specificity of oxidative stress-associated biomarkers to AD pathology by the identification of oxidatively damaged pathology-specific proteins. In this review, we discuss the potential combined diagnostic value of these reported biomarkers in the context of AD and discuss eight oxidative stress-related mRNA biomarkers in AD that we newly identified using a transcriptomics approach. We review these genes in the context of their reported involvement in oxidative stress regulation and specificity for AD. Further research is warranted to establish the protein levels and their functionalities as well as the molecular mechanisms by which these potential biomarkers are involved in regulation of oxidative stress levels and their potential for determination of oxidative stress and disease status of AD patients.

False

CitationGPTRetr11371

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Elevated 4-hydroxynonenal in ventricular fluid in Alzheimer's disease. Abstract of the paper: 4-Hydroxynonenal (4-HNE), an aldehyde by-product of the peroxidation of fatty acids, has been shown to have toxic properties for neurons in culture. In light of increasing evidence that oxidative stress contributes to the neurodegenerative process in Alzheimer's disease (AD), we quantified levels of free and protein-bound 4-HNE in the ventricular fluid from 19 AD subjects and 13 control subjects by high-pressure liquid chromatography and dot-blot immunoassay. Free 4-HNE levels were found to be significantly elevated in the ventricular fluid of AD subjects compared with control subjects (p = 0.0096). These results demonstrate increased lipid peroxidation in AD brain and suggest a role for 4-HNE in the neurodegenerative process.

False

CitationGPTRetr11372

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Evidence of neuronal oxidative damage in Alzheimer's disease. Abstract of the paper: Oxidative stress has been proposed as a pathogenetic mechanism in Alzheimer's disease. One mechanism of oxidative damage is the nitration of tyrosine residues in proteins, mediated by peroxynitrite breakdown. Peroxynitrite, a reaction product of nitric oxide and superoxide radicals, has been implicated in N-methyl-D-aspartate receptor-mediated excitotoxic damage. Reported evidence of oxidative stress in Alzheimer's disease includes increased iron, alterations in protective enzymes, and markers of oxidative damage to proteins and lipids. In this report, we demonstrate the presence of nitrotyrosine in neurofibrillary tangles of Alzheimer's disease. Nitrotyrosine was not detected in controls lacking neurofibrillary tangles. Immunolabeling was demonstrated to be specific nitrotyrosine in a series of control experiments. These observations link oxidative stress with a key pathological lesion of Alzheimer's disease, the neurofibrillary tangle, and demonstrate a pathogenetic mechanism in common with the other major neurodegenerative diseases of aging, Parkinson's disease and amyotrophic lateral sclerosis. These findings further implicate nitric oxide expression and excitotoxicity in the pathogenesis of cell death in Alzheimer's disease.

False

CitationGPTRetr11373

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Proteomic identification of HNE-bound proteins in early Alzheimer disease: Insights into the role of lipid peroxidation in the progression of AD. Abstract of the paper: Early Alzheimer's disease (EAD) is the intermediary stage between mild cognitive impairment (MCI) and late-stage Alzheimer's disease (AD). The symptoms of EAD mirror the disease advancement between the two phases. Dementia, memory deficits, and cognitive decline are more pronounced as the disease progresses. Oxidative stress in brain is reported in MCI and AD, including lipid peroxidation indexed by protein-bound 4-hydroxy-2-nonenal (HNE). There are limited data regarding the proteomics analysis of brain from subjects with EAD and even less concerning the possible relationship of EAD HNE-modified brain proteins with HNE-modified proteins in MCI and AD. Proteomics was utilized to investigate excessively HNE-bound brain proteins in EAD compared to those in control. These new results provide potentially valuable insight into connecting HNE-bound brain proteins in EAD to those previously identified in MCI and AD, since EAD is a transitional stage between MCI and late-stage AD. In total, six proteins were found to be excessively covalently bound by HNE in EAD inferior parietal lobule (IPL) compared to age-related control brain. These proteins play roles in antioxidant defense (manganese superoxide dismutase), neuronal communication and neurite outgrowth (dihydropyriminidase-related protein 2), and energy metabolism (alpha-enolase, malate dehydrogenase, triosephosphate isomerase, and F1 ATPase, alpha subunit). This study shows that there is an overlap of brain proteins in EAD with previously identified oxidatively modified proteins in MCI and late-stage AD. The results are consistent with the hypothesis that oxidative stress, in particular lipid peroxidation, is an early event in the progression of AD, and is the first to identify in EAD identical brain proteins previously identified as HNE-modified in MCI and late-state AD.

False

CitationGPTRetr11374

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Proteomic analysis of protein oxidation in Alzheimer's disease brain. Abstract of the paper: There is a growing body of evidence that oxidative stress plays a major role in Alzheimer's disease (AD) pathogenesis. Identification of oxidatively altered proteins in AD is important for understanding the relationship between protein oxidation, protein aggregation and neurodegeneration. In this communication, we report a method that can be applied to study oxidative changes of individual proteins in brain. In order to analyze protein oxidation by detection of protein-bound carbonyls, cytosolic protein extracts were derivatized with 2,4-dinitrophenylhydrazine (DNPH) and then separated by two-dimensional (2-D) gel electrophoresis. After electrotransfer to polyvinylidene difluoride (PVDF) membranes, proteins were first stained with Sypro Ruby protein stain, and then the oxidized proteins were detected with anti-dinitrophenyl (DNP) antibody. About 150 proteins and more than 100 oxidized proteins were detected and quantified in both AD and control cases by 2-D image analysis. The amount of protein-bound carbonyls was decreased for six and increased for one protein in AD. The amount of protein was increased for three proteins in AD. Furthermore, the degree of oxidation was calculated as the ratio of protein-bound carbonyls to the total amount of an individual protein. Two proteins showed a significant decrease in the degree of oxidation in AD. Our results suggest that the balance of protein oxidation and degradation is altered in AD.

False

CitationGPTRetr11375

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: 4-Hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer's disease. Abstract of the paper: Recent studies have demonstrated oxidative damage is one of the salient features of Alzheimer's disease (AD). In these studies, glycoxidation adduction to and direct oxidation of amino acid side chains have been demonstrated in the lesions and neurons of AD. To address whether lipid damage may also play an important pathogenic role, we raised rabbit antisera specific for the lysine-derived pyrrole adducts formed by lipid peroxidation-derived 4-hydroxynonenal (HNE). These antibodies were used in immunocytochemical evaluation of brain tissue from AD and age-matched control patients. HNE-pyrrole immunoreactivity not only was identified in about half of all neurofibrillary tangles, but was also evident in neurons lacking neurofibrillary tangles in the AD cases. In contrast, few senile plaques were labeled, and then only the dystrophic neurites were weakly stained, whereas the amyloid-beta deposits were unlabeled. Age-matched controls showed only background HNE-pyrrole immunoreactivity in hippocampal or cortical neurons. In addition to providing further evidence that oxidative stress-related protein modification is a pervasive factor in AD, the known neurotoxicity of HNE suggests that lipid peroxidation may also play a role in the neuronal death in AD that underlies cognitive deficits.

False

CitationGPTRetr11376

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: 4-Hydroxynonenal in the pathogenesis and progression of human diseases. Abstract of the paper: Metastable aldehydes produced by lipid peroxidation act as 'toxic second messengers' that extend the injurious potential of free radicals. 4-hydroxy 2-nonenal (HNE), a highly toxic and most abundant stable end product of lipid peroxidation, has been implicated in the tissue damage, dysfunction, injury associated with aging and other pathological states such as cancer, Alzheimer, diabetes, cardiovascular and inflammatory complications. Further, HNE has been considered as a oxidative stress marker and it act as a secondary signaling molecule to regulates a number of cell signaling pathways. Biological activity of HNE depends on its intracellular concentration, which can differentially modulate cell death, growth and differentiation. Therefore, the mechanisms responsible for maintaining the intracellular levels of HNE are most important, not only in the defense against oxidative stress but also in the pathophysiology of a number of disease processes. In this review, we discussed the significance of HNE in mediating various disease processes and how regulation of its metabolism could be therapeutically effective.

False

CitationGPTRetr11377

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Proteomic identification of nitrated brain proteins in amnestic mild cognitive impairment: a regional study. Abstract of the paper: Oxidative stress is an imbalance between the level of antioxidants and oxidants in a cell. Oxidative stress has been shown in brain of subjects with mild cognitive impairment (MCI) as well Alzheimer's disease (AD). MCI is considered as a transition phase between control and AD. The focus of the current study was to identify nitrated proteins in the hippocampus and inferior parietal lobule (IPL) brain regions of subjects with amnestic MCI using proteomics. The identified nitrated proteins in MCI brain were compared to those previously reported to be nitrated and oxidatively modified in AD brain, a comparison that might provide an invaluable insight into the progression of the disease.

False

CitationGPTRetr11378

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Role of oxidative stress in Alzheimer's disease. Abstract of the paper: Alzheimer's disease (AD) is the most common cause of disability in individuals aged >65 years worldwide. AD is characterized by the abnormal deposition of amyloid β (Aβ) peptide, and intracellular accumulation of neurofibrillary tangles of hyperphosphorylated τ protein and dementia. The neurotoxic oligomer Aβ peptide, which is the neuropathological diagnostic criterion of the disease, together with τ protein, are mediators of the neurodegeneration that is among the main causative factors. However, these phenomena are mainly initiated and enhanced by oxidative stress, a process referring to an imbalance between antioxidants and oxidants in favour of oxidants. This imbalance can occur as a result of increased free radicals or a decrease in antioxidant defense, free radicals being a species that contains one or more unpaired electrons in its outer shell. The major source of potent free radicals is the reduction of molecular oxygen in water, that initially yields the superoxide radical, which produces hydrogen peroxide by the addition of an electron. The reduction of hydrogen peroxide produces highly reactive hydroxyl radicals, termed reactive oxygen species (ROS) that can react with lipids, proteins, nucleic acids, and other molecules and may also alter their structures and functions. Thus, tissues and organs, particularly the brain, a vulnerable organ, are affected by ROS due to its composition. The brain is largely composed of easily oxidizable lipids while featuring a high oxygen consumption rate. The current review examined the role of oxidative stress in AD.

False

CitationGPTRetr11379

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: 4hydroxy2nonenal hne a product of lipid peroxidation which by michael addiction is able to bind proteins 3nitrotyrosine 3nt a product of protein nitration and protein carbonyl pc derived from protein oxidation were measured using dot blot technique Title of the paper: Histochemical detection of 4-hydroxynonenal protein in Alzheimer amyloid. Abstract of the paper: The presence of lipid peroxidation product in amyloid deposits from seven patients with Alzheimer disease and nine with non-Alzheimer disease was examined immunohistochemically by means of an affinity purified anti-HNE antibody to hydroxynonenal (HNE), a marker of lipid peroxidation. A positive reaction was found in amyloid deposits in all the specimens examined: most of the perivascular areas (89%) where amyloid deposition was confirmed by Congo red staining, showed immunoreactivity with the antibody in the specimens of Alzheimer disease. Twenty-one percent of senile plaques which were also stained by Congo red staining reacted with this antibody. Several perivascular cells were also stained by anti-HNE antibody. In other neurons both in Alzheimer and non-Alzheimer disease patients, only a few percent reacted with this antibody and no statistical difference was observed between them. These results verify that lipid peroxidation via free radical injury occurs in amyloid deposits in Alzheimer amyloid. Since HNE has been identified as a cytotoxic metabolite of free radical injury, amyloid deposits in the tissue may exhibit a toxic effect during the generation process of HNE.

False

CitationGPTRetr11380

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: The nicotinic acetylcholine receptor: smoking and Alzheimer's disease revisited. Abstract of the paper: Epidemiological studies regarding Alzheimer's disease (AD) in smokers currently suggest inconsistent results. The clinicopathological findings also vary as to how AD pathology is affected by smoking behavior. Even though clinicopathological, functional, and epidemiological studies in humans do not present a consistent picture, much of the in vitro data implies that nicotine has neuroprotective effects when used in neurodegenerative disorder models. Current studies of the effects of nicotine and nicotinic agonists on cognitive function in both the non-demented and those with AD are not convincing. More data is needed to determine whether repetitive activation of nAChR with intermittent or acute exposure to nicotine, acute activation of nAChR, or long-lasting inactivation of nAChR secondary to chronic nicotine exposure will have a therapeutic effect and/or explain the beneficial effects of those types of drugs. Other studies show multifaceted connections between nicotine, nicotinic agonists, smoking, and nAChRs implicated in AD etiology. Although many controversies still exist, ongoing studies are revealing how nicotinic receptor changes and functions may be significant to the neurochemical, pathological, and clinical changes that appear in AD.

False

CitationGPTRetr11381

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Cognitive effects of nicotine. Abstract of the paper: Nicotine and other nicotinic agonists have been found to improve performance on attention and memory tasks. Clinical studies using nicotine skin patches have demonstrated the efficacy of nicotine in treating cognitive impairments associated with Alzheimer's disease, schizophrenia, and attention-deficit/hyperactivity disorder. Experimental animal studies have demonstrated the persistence of nicotine-induced working memory improvement with chronic exposure, in addition to the efficacy of a variety of nicotinic agonists. Mechanistic studies have found that alpha7 and alpha4beta2 nicotinic receptors in the hippocampus are critical for nicotinic involvement in cognitive function. Clinical and experimental animal studies provide mutually supporting information for the development of novel nicotinic therapies for cognitive dysfunction.

False

CitationGPTRetr11382

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Stress and the α7 nicotinic acetylcholine receptor. Abstract of the paper: Nicotine is well known for its deleterious effects on human health, and it has long been known that nicotine interacts with the stress axis in both man and in laboratory animals. Nicotine also has beneficial effects upon cognition, and an emerging literature has demonstrated that it may play a protective or palliative role in diseases such as Alzheimer's disease and schizophrenia. Recent advances have permitted scientists to identify the specific subtypes of nicotinic receptors responsible for the drugs varied physiological effects. The α7 subunit of the nicotinic acetylcholine receptor (NAchRα7), has been identified as a significant mediator of nicotine's interactions with the stress axis and human disease. The NAchRα7 has also been shown to have neuroprotective effects via multiple pathways, making it a logical target for the treatment of a number of brain disorders.

False

CitationGPTRetr11383

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Intensification of long-term memory deficit by chronic stress and prevention by nicotine in a rat model of Alzheimer's disease. Abstract of the paper: Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cholinergic dysfunction and deposition of beta-amyloid (Aβ) in regions of the brain associated with learning and memory. The sporadic nature and late onset of most AD cases suggests that aside from biological determinants, environmental factors such as stress may also play a role in the progression of the disease. Behavioral and molecular studies were utilized to evaluate the effects of chronic nicotine treatment in the prevention of impairment of long-term memory. The rat model of AD was induced by i.c.v. osmotic pump infusion of Aβ peptides. Chronic psychosocial stress and chronic nicotine treatment were instituted for 6weeks. Spatial memory testing in the Radial Arm Water Maze revealed that, although stress, by itself, did not affect long-term memory, the combination of chronic stress and Aβ infusion impaired long-term memory significantly more than Aβ peptides infusion alone. Chronic nicotine treatment completely prevented Aβ- and stress/Aβ combination-induced memory impairment. Furthermore, molecular findings in hippocampal CA1 region of stress/Aβ rats indicated marked reduction in the protein levels of phosphorylated cAMP response element binding (p-CREB) and calcium-calmodulin-dependent protein kinase IV (CaMKIV), with significant increases in the levels of brain-derived neurotrophic factor (BDNF). These disturbances in signaling pathways, which may be the underlying mechanisms of impairment of long-term memory in these rats, were totally prevented by chronic nicotine treatment.

False

CitationGPTRetr11384

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotine patches in Alzheimer's disease: pilot study on learning, memory, and safety. Abstract of the paper: In view of the cholinergic deficits present in patients with Alzheimer's disease (AD), a widely investigated treatment strategy for the cognitive deficits in AD is cholinergic stimulation. Although nicotinic cholinergic receptor binding has been demonstrated to be deficient in the AD brain, the predominant theoretical and therapeutic focus to date has been on muscarinic cholinergic receptors and systems. The purpose of the present study was to evaluate the effects of sustained nicotine administration on behavior, cognition, and physiology. A double-blind placebo-controlled trial was conducted in which six patients with probable AD were exposed to 7, 8, and 7 days of placebo, nicotine, and washout, respectively. Daily sessions evaluating learning, memory, and behavior were conducted. Global cognitive functioning, rest and activity levels, cardiac activity, and blood levels were also measured. Findings included improved learning during the nicotine condition, which persisted throughout washout. Memory, behavior, and global cognition were not significantly affected. Sustained administration of nicotine appeared to be safe, although sleep showed a significant decrease.

False

CitationGPTRetr11385

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotinic system involvement in Alzheimer's and Parkinson's diseases. Implications for therapeutics. Abstract of the paper: Advances in our understanding of the structure, function and distribution of nicotinic acetylcholine receptors in the CNS have provided the impetus for new studies examining the role(s) that these receptors and associated processes may play in CNS functions. Further motivation has come from the realisation that such receptors must be involved in the maintenance of cigarette smoking, and from clues provided by studies of degenerative neurological diseases such as Alzheimer's disease and Parkinson's disease, in which the loss of nicotinic receptors has been described. Ongoing investigations of the molecular substructure of central nicotinic receptors and their pharmacology have begun to open up new possibilities for novel CNS therapeutics with nicotinic agents. Exploiting these possibilities will require understanding of the role(s) that these receptor systems play in human cognitive, behavioural, motor and sensory functioning. Clues from careful studies of human cognition are beginning to emerge and will provide direction for studies of potentially therapeutic novel nicotinic agents. Despite the promising results of acute studies, few long term studies with nicotine or nicotinic drugs have been performed in dementing disorders. Thus there is uncertainty as to whether long term nicotinic treatment will provide sustained cognitive benefit. It is even more uncertain whether such cognitive benefit will have a significant clinical impact on patients and their families. To maximise the potential benefit of long term treatment with nicotinic agonists (or other cholinergic drugs), we suggest that drug treatment should be combined with cognitive rehabilitation strategies. This will enable patients and/or their families to focus on the particular cognitive domains that may be improved.

False

CitationGPTRetr11386

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Chronic nicotine restores normal Aβ levels and prevents short-term memory and E-LTP impairment in Aβ rat model of Alzheimer's disease. Abstract of the paper: Alzheimer's disease (AD) is a devastating neurodegenerative disorder characterized by increased deposition of beta-amyloid (Aβ) peptides and progressive cholinergic dysfunction in regions of the brain involved in learning and memory processing. In AD, progressive accumulation of Aβ peptide impairs nicotinic acetylcholine receptor (nAChR) function by an unknown mechanism believed to involve α(7)- and α(4)β(2)-nAChR blockade. The three approaches of the current study evaluated the effects of chronic nicotine treatment in the prevention of Aβ-induced impairment of learning and short-term memory. Rat AD model was induced by 14-day i.c.v. osmotic pump infusion of a 1:1 mixture of 300 pmol/day Aβ(1-40)/Aβ(1-42) or Aβ(40-1) (inactive peptide, control). The effect of nicotine (2 mg/(kg day)) on Aβ-induced spatial learning and memory impairments was assessed by evaluation of performance in the radial arm water maze (RAWM), in vivo electrophysiological recordings of early-phase long-term potentiation (E-LTP) in urethane-anesthetized rats, and immunoblot analysis to determine changes in the levels of beta-site amyloid precursor protein (APP)-cleaving enzyme (BACE), Aβ and memory-related proteins. The results indicate that 6 weeks of nicotine treatment reduced the levels of Aβ(1-40) and BACE1 peptides in hippocampal area CA1 and prevented Aβ-induced impairment of learning and short-term memory. Chronic nicotine also prevented the Aβ-induced inhibition of basal synaptic transmission and LTP in hippocampal area CA1. Furthermore, chronic nicotine treatment prevented the Aβ-induced reduction of α(7)- and α(4)-nAChR. These effects of nicotine may be due, at least in part, to upregulation of brain derived neurotropic factor (BDNF).

True

CitationGPTRetr11387

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotinic effects on cognitive function: behavioral characterization, pharmacological specification, and anatomic localization. Abstract of the paper: RATIONALE Nicotine has been shown in a variety of studies in humans and experimental animals to improve cognitive function. Nicotinic treatments are being developed as therapeutic treatments for cognitive dysfunction. OBJECTIVES Critical for the development of nicotinic therapeutics is an understanding of the neurobehavioral bases for nicotinic involvement in cognitive function. METHODS Specific and diverse cognitive functions affected by nicotinic treatments are reviewed, including attention, learning, and memory. The neural substrates for these behavioral actions involve the identification of the critical pharmacologic receptor targets, in particular brain locations, and how those incipient targets integrate with broader neural systems involved with cognitive function. RESULTS Nicotine and nicotinic agonists can improve working memory function, learning, and attention. Both alpha4beta2 and alpha7 nicotinic receptors appear to be critical for memory function. The hippocampus and the amygdala in particular have been found to be important for memory, with decreased nicotinic activity in these areas impairing memory. Nicotine and nicotinic analogs have shown promise for inducing cognitive improvement. Positive therapeutic effects have been seen in initial studies with a variety of cognitive dysfunctions, including Alzheimer's disease, age-associated memory impairment, schizophrenia, and attention deficit hyperactivity disorder. CONCLUSIONS Discovery of the behavioral, pharmacological, and anatomic specificity of nicotinic effects on learning, memory, and attention not only aids the understanding of nicotinic involvement in the basis of cognitive function, but also helps in the development of novel nicotinic treatments for cognitive dysfunction. Nicotinic treatments directed at specific receptor subtypes and nicotinic cotreatments with drugs affecting interacting transmitter systems may provide cognitive benefits most relevant to different syndromes of cognitive impairment such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder. Further research is necessary in order to determine the efficacy and safety of nicotinic treatments of these cognitive disorders.

False

CitationGPTRetr11388

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotinic receptor subtypes and cognitive function. Abstract of the paper: Nicotinic receptor systems are involved in a wide variety of behavioral functions including cognitive function. Nicotinic medications may provide beneficial treatment for cognitive dysfunction such as Alzheimer's disease, schizophrenia, and attention deficit hyperactivity disorder (ADHD). Nicotine has been shown to improve attentional performance in all of these disorders. Better efficacy with fewer side effects might be achieved with novel nicotinic ligands selective for particular nicotinic subtypes. To develop these novel selective nicotinic ligands it is important to use animal models to determine the critical neurobehavioral bases for nicotinic involvement in cognitive function. Nicotine-induced cognitive improvement in rats is most consistently seen in working memory tasks. We have found that both acute and chronic nicotine administration significantly improves working memory performance of rats in the radial-arm maze. The pharmacologic and anatomic mechanisms for this effect have been examined in our laboratory in a series of local drug infusion studies. Both alpha 4 beta 2 and alpha 7 nicotinic receptors in the ventral hippocampus and basolateral amygdala are involved in working memory function. Working memory impairments were caused by local infusion of either alpha 4 beta 2 or alpha 7 antagonists. Ventral hippocampal alpha 4 beta 2 blockade-induced working memory deficits are reversed by chronic systemic nicotine treatment, while ventral hippocampal alpha 7 blockade-induced working memory deficits were not found to be reversed by the same nicotine regimen. Interestingly, alpha 4 beta 2 and alpha 7 induced deficits were not found to be additive in either the ventral hippocampus or the basolateral amygdala. In fact, in the amygdala, alpha 7 antagonist cotreatment actually reversed the working memory impairment caused by alpha 4 beta 2 antagonist administration. These studies of the neural nicotinic mechanisms underlying cognitive function are key for opening avenues for development of safe and effective nicotinic treatments for cognitive dysfunction.

False

CitationGPTRetr11389

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Chronic stress and Alzheimer's disease-like pathogenesis in a rat model: prevention by nicotine. Abstract of the paper: Environmental factors including chronic stress may play a critical role in the manifestation of Alzheimer's disease (AD).This review summarizes our studies of the aggravation of the impaired cognitive ability and its cellular and molecular correlates by chronic psychosocial stress and prevention by nicotine in an Aβ rat model of AD. We utilized three approaches: learning and memory tests in the radial arm water maze, electrophysiological recordings of the cellular correlates of memory, long-term potentiation (LTP) and long-term depression (LTD), in anesthetized rats, and immunoblot analysis of synaptic plasticity- and cognition-related signaling molecules. The Aβ rat model, representing the sporadic form of established AD, was induced by continuous i.c.v. infusion of a pathogenic dose of Aβ peptides via a 14- day osmotic pump. In this AD model, chronic stress intensified cognitive deficits, accentuated the disruption of signaling molecules levels and produced greater depression of LTP than what was seen with Aβ infusion alone. Chronic treatment with nicotine was highly efficient in preventing the effects of Aβ infusion and the exacerbating impact of chronic stress. Possible mechanisms for the effect of chronic stress are discussed.

False

CitationGPTRetr11390

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotinic Acetylcholine Receptor Agonists for the Treatment of Alzheimer's Dementia: An Update. Abstract of the paper: A significant portion of the clinical phenotype observed in Alzheimer's disease (AD) occurs through nicotinic acetylcholine receptors (nAChRs). Degeneration of cholinergic neurons, combined with aberrant nAChR expression and activation partially through amyloid-beta peptide (Aβ)-nAChR leads to upregulation of pro-inflammatory pathways and subsequently the progressive cognitive decline of AD. Interestingly, the cholinergic anti-inflammatory pathway is also mediated through nAChR particularly α7 nAChR. Thus, agonists of these receptors will likely exert pro-cognitive benefits through multiple mechanisms including stimulating the cholinergic pathway, modulating inflammation, and buffering the effects of amyloid. Despite this promising theoretical use, trials thus far have been complicated by adverse effects or minimal improvement. This review will provide an update on several pharmacological nAChR agonists tested in clinical trials and reasons that further investigation of nAChR agonists is merited. IMPLICATIONS nAChRs have consistently presented a promising theoretical use in the treatment of AD; however, trials thus far have been complicated by adverse effects or minimal improvement. This review will provide an update on several pharmacological nAChR agonists trialed and reasons that further investigation of nAChR agonists is merited.

False

CitationGPTRetr11391

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Revisiting nicotine's role in the ageing brain and cognitive impairment. Abstract of the paper: Brain ageing is a complex process which in its pathologic form is associated with learning and memory dysfunction or cognitive impairment. During ageing, changes in cholinergic innervations and reduced acetylcholinergic tonus may trigger a series of molecular pathways participating in oxidative stress, excitotoxicity, amyloid-β toxicity, apoptosis, neuroinflammation, and perturb neurotrophic factors in the brain. Nicotine is an exogenous agonist of nicotinic acetylcholine receptors (nAChRs) and acts as a pharmacological chaperone in the regulation of nAChR expression, potentially intervening in age-related changes in diverse molecular pathways leading to pathology. Although nicotine has therapeutic potential, paradoxical effects have been reported, possibly due to its inverted U-shape dose-response effects or pharmacokinetic factors. Additionally, nicotine administration should result in optimum therapeutic effects without imparting abuse potential or toxicity. Overall, this review aims to compile the previous and most recent data on nicotine and its effects on cognition-related mechanisms and age-related cognitive impairment.

False

CitationGPTRetr11392

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Modulation of hippocampus-dependent learning and synaptic plasticity by nicotine. Abstract of the paper: A long-standing relationship between nicotinic acetylcholine receptors (nAChRs) and cognition exists. Drugs that act at nAChRs can have cognitive-enhancing effects and diseases that disrupt cognition such as Alzheimer's disease and schizophrenia are associated with altered nAChR function. Specifically, hippocampus-dependent learning is particularly sensitive to the effects of nicotine. However, the effects of nicotine on hippocampus-dependent learning vary not only with the doses of nicotine used and whether nicotine is administered acutely, chronically, or withdrawn after chronic nicotine treatment but also vary across different hippocampus-dependent tasks such as the Morris water maze, the radial arm maze, and contextual fear conditioning. In addition, nicotine has variable effects across different types of hippocampal long-term potentiation (LTP). Because different types of hippocampus-dependent learning and LTP involve different neural and molecular substrates, comparing the effects of nicotine across these paradigms can yield insights into the mechanisms that may underlie the effects of nicotine on learning and memory and aid in understanding the variable effects of nicotine on cognitive processes. This review compares and contrasts the effects of nicotine on hippocampus-dependent learning and LTP and briefly discusses how the effects of nicotine on learning could contribute to nicotine addiction.

False

CitationGPTRetr11393

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotine, brain nicotinic receptors, and neuropsychiatric disorders. Abstract of the paper: Neuronal nicotinic acetylcholine receptors (nAChRs) represent a large family of ligand-gated cation channels with diverse structures and properties. In contrast to the muscular nAChRs, the physiological functions of neuronal nAChRs are not well defined to date. Behavioral studies indicate that brain nAChRs participate in complex functions such as attention, memory, and cognition, whereas clinical data suggest their involvement in the pathogenesis of certain neuropsychiatric disorders (Alzheimer's and Parkinson's diseases, Tourette's syndrome, schizophrenia, depression, etc.). For the majority of these disorders, the use of nAChRs' agonists may represent either a prophylactic (especially for Alzheimer's and Parkinson's diseases) or a symptomatic treatment. The possible mechanisms underlying these beneficial effects as well as the characteristics and potential therapeutic use of new, subtype-selective nAChRs agonists are presented.

False

CitationGPTRetr11394

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Selective changes in nicotinic acetylcholine receptor subtypes related to tobacco smoking: an immunohistochemical study. Abstract of the paper: Increases in neuronal nicotinic receptors (nAChRs) in response to nicotine exposure have been reported in cell cultures, rodent brains, and in the brains of human smokers. The present study examines alterations in alpha4 and alpha7 nAChR subunit cellular expression in human hippocampus and entorhinal cortex from normal elderly individuals with known smoking history. There were significant increases in the intensity of alpha4 immunoreactive neuropil, but not the number of cell bodies, in many regions of hippocampus and entorhinal cortex in smokers compared to age-matched non-smokers and ex-smokers. There was also an increase in alpha7 immunoreactive perikarya in the granular cell layer of dentate gyrus in smokers but not other regions examined. There was, in contrast, a significant reduction in alpha7 immunoreactive astrocytes in smokers and ex-smokers compared to non-smokers. These findings suggest exposure to tobacco smoke acutely up-regulates alpha4 receptors in axon terminals and dendrites but not perikarya, whereas tobacco smoking induced down-regulation of alpha7 expression on astrocytes is a long-term effect. As the alpha4 subunit decreases with ageing and degenerative diseases such as Alzheimer's disease, whereas alpha7 increases in astrocytes in Alzheimer's disease, the findings further indicate the therapeutic relevance of nicotinic agonists such as nicotine.

False

CitationGPTRetr11395

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Relationship between nicotinic receptors and cognitive function in early Alzheimer's disease: a 2-[18F]fluoro-A-85380 PET study. Abstract of the paper: Neuronal nicotinic acetylcholine receptors (nAChRs) are critical for higher order cognitive processes. Post-mortem studies suggest reductions in nAChRs (particularly the alpha(4)beta(2) subtype) with ageing and in Alzheimer's disease (AD). This study aimed to; (1) quantify nAChR distribution in vivo with 2-[18F]fluoro-A-85380 (2-FA) in 15 early AD patients compared to 14 age-matched, healthy controls (HC) and (2) correlate nAChR distribution with cognitive performance in both groups. All participants were non-smokers and underwent cognitive testing along with a dynamic PET scan after injection of 200 MBq of 2-FA. Brain regional 2-FA binding was assessed through a simplified estimation of Distribution Volume (DV(S)). The AD group differed significantly from HC on all cognitive measures employed, with impairments on measures of attention, working memory, language, executive function, visuospatial ability, verbal learning and verbal memory (p<.05). Contrary to post-mortem data this study found no evidence of in vivo nAChR loss in early AD despite significant cognitive impairment. Furthermore, no correlation between nAChR and cognitive performance was found for either group. The findings of the current study suggest preservation of nAChRs early in AD supporting previous studies. It is possible that while the clinical 2-FA PET method described here may be insensitive in detecting changes in early AD, such changes may be detected in more advanced stages of the illness.

False

CitationGPTRetr11396

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotinic receptors, amyloid-beta, and synaptic failure in Alzheimer's disease. Abstract of the paper: Dysfunctional cholinergic transmission is thought to underlie, at least in part, memory impairment and cognitive deficits in Alzheimer's disease (AD). However, it is still unclear whether this is a consequence of the loss of cholinergic neurons and elimination of nicotinic acetycholine receptors (nAChRs) in AD brain or of a direct impact of molecular interactions of the amyloid-beta (Abeta) peptide with nAChRs, leading to dysregulation of receptor function. This review examines recent progress in our understanding of the roles of nicotinic receptors in mechanisms of synaptic plasticity, molecular interactions of Abeta with nAChRs, and how Abeta-induced dysregulation of nicotinic receptor function may underlie synaptic failure in AD.

False

CitationGPTRetr11397

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Chronic nicotine treatment reduces beta-amyloidosis in the brain of a mouse model of Alzheimer's disease (APPsw). Abstract of the paper: Alzheimer's disease neuropathology is characterised by beta-amyloid plaques and neurofibrillary tangles. Inhibition of beta-amyloid accumulation may be essential for effective therapy in Alzheimer's disease. In this study we have treated transgenic mice carrying the Swedish mutation of human amyloid precursor protein [Tg(Hu.APP695.K670N-M671L)2576], which develop brain beta-amyloid deposits, with nicotine in drinking fluid (200 microg/mL) from 9-14.5 months of age (5.5 months). A significant reduction in amyloid beta peptide 1-42 positive plaques by more than 80% (p < 0.03) was observed in the brains of nicotine treated compared to sucrose treated transgenic mice. In addition, there was a selective reduction in extractable amyloid beta peptides in nicotine treated mice; cortical insoluble 1-40 and 1-42 peptide levels were lower by 48 and 60%, respectively (p < 0.005), whilst there was no significant change in soluble 1-40 or 1-42 levels. The expression of glial fibrillary acidic protein was not affected by nicotine treatment. These results indicate that nicotine may effectively reduce amyloid beta peptide aggregation in brain and that nicotinic drug treatment may be a novel protective therapy in Alzheimer's disease.

False

CitationGPTRetr11398

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Nicotine attenuates beta-amyloid peptide-induced neurotoxicity, free radical and calcium accumulation in hippocampal neuronal cultures. Abstract of the paper: 1. Recent studies indicate that neuronal loss in Alzheimer's disease (AD) is accompanied by the deposition of beta-amyloid protein (A beta) in senile plaques. Nicotine as a major component of cigarette smoke has been suggested to have a protective effect for neurons against A beta neurotoxicity. 2. Our present study demonstrates that nicotine protected cultured hippocampal neurons against the A beta-induced apoptosis. Nicotine effectively inhibits apoptosis in hippocampal cultures caused by A beta(25-35) or A beta(1-40) treatment and increase of caspase activity induced by A beta(25-35) or A beta(1-40). 3. Measurements of cellular oxidation and intracellular free Ca(2+) showed that nicotine suppressed A beta-induced accumulation of free radical and increase of intracellular free Ca(2+). 4. Cholinergic antagonist mecamylamine inhibited nicotine-induced protection against A beta-induced caspase-3 activation and ROS accumulation. 5. The data show that the protection of nicotine is partly via nicotinic receptors. Our results suggest that nicotine may be beneficial in retarding the neurodegenerative diseases such as AD.

False

CitationGPTRetr11399

Predict the citation correlation between the following sentence and a biomedical paper represented by the provided title and abstract. Sentence: laboratory and clinical studies have shown that nicotine improves cognitive function in ad patients and attenuates aβinduced amnesia in rodents 19 40 44 45the finding that chronic nicotine treatment prevents stressinduced down regulation of central nicotinic acetylcholine receptors nachrs suggests a mechanism by which nicotine may prevent stressinduced impairment of memory and ltp Title of the paper: Chronic nicotine treatment decreases LPS signaling through NF-κB and TLR-4 modulation in the hippocampus. Abstract of the paper: The hippocampus is a brain region that is rich in nicotinic acetylcholine receptors (nAChRs), especially the α7 subtype. The hippocampus is severely affected in disorders that have a neuroinflammatory component, such as Alzheimer's disease, Parkinson's disease, and schizophrenia. Previous studies demonstrated both in vivo and in vitro that nicotine inhibits immunological responses, including those that are triggered by the inflammatory agent lipopolysaccharide (LPS), the endotoxin of Gram-negative bacteria. The present study investigated whether chronically administered nicotine interferes with the nuclear binding of nuclear factor-κB (NF-κB) and the expression of LPS-induced inflammatory response genes. The results indicated that chronic nicotine administration (0.1mg/kg, s.c., 14days) inhibited the LPS-induced nuclear binding of NF-κB and mRNA expression levels of Tnf, Il1b, Nos2, and Tlr4. The presence of both the selective α7 nAChR antagonist methyllycaconitine (MLA; 5.0mg/kg i.p., 14days) and the nonselective nAChR antagonist mecamylamine (Meca; 1.0mg/kg, s.c., 14days) reversed the inhibitory effects of nicotine. These results suggest that the chronic activation of α7- and αxβy-containing nAChRs reduces acute inflammatory responses in the brain.

False