rudyvdbrink/CitationDatabase huggingface dataset:
Control of response interference: caudate nucleus contributes to selective inhibition.
Scientific reports, 2020

While the role of cortical regions in cognitive control processes is well accepted, the contribution of subcortical structures (e.g., the striatum), especially to the control of response interference, remains controversial. Therefore, the present study aimed to investigate the cortical and particularly subcortical neural mechanisms of response interference control (including selective inhibition). Thirteen healthy young participants underwent event-related functional magnetic resonance imaging while performing a unimanual version of the Simon task. In this task, successful performance required the resolution of stimulus-response conflicts in incongruent trials by selectively inhibiting interfering response tendencies. The behavioral results show an asymmetrical Simon effect that was more pronounced in the contralateral hemifield. Contrasting incongruent trials with congruent trials (i.e., the overall Simon effect) significantly activated clusters in the right anterior cingulate cortex, the right posterior insula, and the caudate nucleus bilaterally. Furthermore, a region of interest analysis based on previous patient studies revealed that activation in the bilateral caudate nucleus significantly co-varied with a parameter of selective inhibition derived from distributional analyses of response times. Our results corroborate the notion that the cognitive control of response interference is supported by a fronto-striatal circuitry, with a functional contribution of the caudate nucleus to the selective inhibition of interfering response tendencies.
Length of Hospital Stay for Hip Fracture and 30-Day Mortality in People With Alzheimer's Disease: A Cohort Study in Finland.
The journals of gerontology. Series A, Biological sciences and medical sciences, 2020

Persons with Alzheimer's disease (AD) are at higher risk of hip fractures (HFs) than general older population and have worse prognosis after HF. Hospital stays after HF have shortened along time. We investigated the association between length of hospital stay after HF and mortality after discharge among persons with AD.
A web based dynamic MANA Nomogram for predicting the malignant cerebral edema in patients with large hemispheric infarction.
BMC neurology, 2020

For large hemispheric infarction (LHI), malignant cerebral edema (MCE) is a life-threatening complication with a mortality rate approaching 80%. Establishing a convenient prediction model of MCE after LHI is vital for the rapid identification of high-risk patients as well as for a better understanding of the potential mechanism underlying MCE.
Acetaminophen disrupts memory in object recognition and increases extracellular signal-regulated kinase phosphorylation in male mice.
Behavioral neuroscience, 2018

Acetaminophen (also known as paracetamol) is a commonly used over-the-counter pain medication, but recent evidence suggests that a single exposure or prenatal exposure may have significant behavioral effects. This investigation aimed to determine whether acetaminophen could disrupt memory formation in an object-recognition task and to quantify potential changes in memory-related signaling cascades in the hippocampus of mice after acetaminophen administration. Using male mice, we examined the effect of a single subcutaneous injection of acetaminophen on the object-recognition task, a single-trial, hippocampus-dependent memory task. We also investigated potential changes in the activation of extracellular signal-regulated kinase (ERK) in the dorsal mouse hippocampus 1 hr after a subcutaneous injection of acetaminophen. We found that 50 mg/kg and 100 mg/kg interfered with performance in the object-recognition memory task, whereas 10 mg/kg did not. We also found that a single 50 mg/kg injection of acetaminophen significantly increased p42 ERK phosphorylation in the dorsal mouse hippocampus. Overall, these results suggest that a single dose of acetaminophen can have significant effects on memory and alters signaling kinases critical for memory consolidation. Further work is needed to determine the involved mechanisms. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
Synaptotagmin-7 deficiency induces mania-like behavioral abnormalities through attenuating GluN2B activity.
Proceedings of the National Academy of Sciences of the United States of America, 2020

Synaptotagmin-7 (Syt7) probably plays an important role in bipolar-like behavioral abnormalities in mice; however, the underlying mechanisms for this have remained elusive. Unlike antidepressants that cause mood overcorrection in bipolar depression,
Neuroscience: To Eat or to Sleep?
Current biology : CB, 2018

Energy and sleep homeostasis are entwined, each capable of exerting priority based on need. The identification of central nodes involved in the appropriate orchestration of these systems is critical to our understanding of how the brain regulates behavior.
Quantifying uncertainty in brain-predicted age using scalar-on-image quantile regression.
NeuroImage, 2020

Prediction of subject age from brain anatomical MRI has the potential to provide a sensitive summary of brain changes, indicative of different neurodegenerative diseases. However, existing studies typically neglect the uncertainty of these predictions. In this work we take into account this uncertainty by applying methods of functional data analysis. We propose a penalised functional quantile regression model of age on brain structure with cognitively normal (CN) subjects in the Alzheimer's Disease Neuroimaging Initiative (ADNI), and use it to predict brain age in Mild Cognitive Impairment (MCI) and Alzheimer's Disease (AD) subjects. Unlike the machine learning approaches available in the literature of brain age prediction, which provide only point predictions, the outcome of our model is a prediction interval for each subject.
Rapid changes in brain activity during learning of grapheme-phoneme associations in adults.
NeuroImage, 2020

Learning to associate written letters with speech sounds is crucial for the initial phase of acquiring reading skills. However, little is known about the cortical reorganization for supporting letter-speech sound learning, particularly the brain dynamics during the learning of grapheme-phoneme associations. In the present study, we trained 30 Finnish participants (mean age: 24.33 years, SD: 3.50 years) to associate novel foreign letters with familiar Finnish speech sounds on two consecutive days (first day ​~ ​50 ​min; second day ​~ ​25 ​min), while neural activity was measured using magnetoencephalography (MEG). Two sets of audiovisual stimuli were used for the training in which the grapheme-phoneme association in one set (Learnable) could be learned based on the different learning cues provided, but not in the other set (Control). The learning progress was tracked at a trial-by-trial basis and used to segment different learning stages for the MEG source analysis. The learning-related changes were examined by comparing the brain responses to Learnable and Control uni/multi-sensory stimuli, as well as the brain responses to learning cues at different learning stages over the two days. We found dynamic changes in brain responses related to multi-sensory processing when grapheme-phoneme associations were learned. Further, changes were observed in the brain responses to the novel letters during the learning process. We also found that some of these learning effects were observed only after memory consolidation the following day. Overall, the learning process modulated the activity in a large network of brain regions, including the superior temporal cortex and the dorsal (parietal) pathway. Most interestingly, middle- and inferior-temporal regions were engaged during multi-sensory memory encoding after the cross-modal relationship was extracted from the learning cues. Our findings highlight the brain dynamics and plasticity related to the learning of letter-speech sound associations and provide a more refined model of grapheme-phoneme learning in reading acquisition.
[Are variations of structural neuro-anatomy promising endophenotype candidates in bipolar disorder?].
L'Encephale, 2012

Bipolar disorder is a complex pathology which has a strong heritability component. Epidemiologic studies have pinpointed the contribution of genetic factors to the heritability component. The molecular studies, that have used classical genetic approaches, have been inconclusive at indentifying genes involved in the etiology of this disorder. To overcome these difficulties, a number of strategies have been developed. One of them is the endophenotypic approach. Its main scope is to identify biological markers that are influenced by genetic factors that are less complex than those involved in the clinical expression of the disorder. Thus, it is likely these markers will be more readily linked to specific genetic loci. In this article, we describe the main phenotypes of neuro-anatomic measurements that are widely used in research, and report data on their heritability in the general population. Then, we focus on the results of the few structural neuro-imaging studies that have been carried out in families of patients suffering of bipolar disorders. The current data converge to indicate that subtle structural abnormalities, particularly at the level white matter tracts, seem to be promising endophenotype candidates for bipolar disorder.
Correction to: Predictors of abatacept retention over 2 years in patients with rheumatoid arthritis: results from the real-world ACTION study.
Clinical rheumatology, 2019

The article listed above was initially published with incorrect copyright information. Upon publication of this Correction, the copyright of this article changed to "The Author(s)". The original article has been corrected.
Cumulative incidences of hospital-treated psychiatric disorders are increasing in five Finnish birth cohorts.
Acta psychiatrica Scandinavica, 2021

The aim of this study was to explore changes in the incidences of childhood and early adulthood hospital-treated psychiatric disorders in five large Finnish birth cohorts of individuals born between 1966 and 1997.
Relatives' perspective on the quality of geriatric care and rehabilitation--development and testing of a questionnaire.
Scandinavian journal of caring sciences, 2008

We perceived a need for relatives' evaluation of geriatric care and rehabilitation during the care period as well as the first few weeks after discharge. The aim of this study was therefore to develop and test a questionnaire for use in telephone interviews with relatives of patients discharged from geriatric wards to measure their perceptions of the quality of care. The instrument development process comprised a literature review, focus group interviews, construction of items, test of content validity, a pilot study and finally the main data collection to test the construct validity and reliability. A Likert-type questionnaire was used containing 26 items with five response alternatives; totally disagree, partly disagree, doubtful, partly agree and totally agree. The main data collection comprised 238 telephone interviews. The factor analysis revealed four factors with an eigenvalue >1.0. Cronbach's alpha coefficient was 0.89, which indicates high reliability. The duration of the telephone interview was approximately 10-20 minutes. The relatives appreciated the opportunity to evaluate the care, and a majority stated that they preferred a telephone interview to answering in writing. The questionnaire is considered reliable, valid and useful for identifying areas in need of quality improvement interventions.
Do Current Measures of Polygenic Risk for Mental Disorders Contribute to Population Variance in Mental Health?
Schizophrenia bulletin, 2020

The polygenic risk score (PRS) allows for quantification of the relative contributions of genes and environment in population-based studies of mental health. We analyzed the impact of transdiagnostic schizophrenia PRS and measures of familial and environmental risk on the level of and change in general mental health (Short-Form-36 mental health) in the Netherlands Mental Health Survey and Incidence Study-2 general population sample, interviewed 4 times over a period of 9 years, yielding 8901 observations in 2380 individuals. Schizophrenia PRS, family history, somatic pain, and a range of environmental risks and social circumstances were included in the regression model of level of and change in mental health. We calculated the relative contribution of each (group of) risk factor(s) to the variance in (change in) mental health. In the combined model, familial and environmental factors explained around 17% of the variance in mental health, of which around 5% was explained by age and sex, 30% by social circumstances, 16% by pain, 22% by environmental risk factors, 24% by family history, and 3% by PRS for schizophrenia (PRS-SZ). Results were similar, but attenuated, for the model of mental health change over time. Childhood trauma and gap between actual and desired social status explained most of the variance. PRS for bipolar disorder, cross-disorder, and depression explained less variance in mental health than PRS-SZ. Polygenic risk for mental suffering, derived from significance-testing in massive samples, lacks impact in analyses focusing on prediction in a general population epidemiological setting. Social-environmental circumstances, particularly childhood trauma and perceived status gap, drive most of the attributable variation in population mental health.
Resection of Large Petrotentorial Tumor via a Retrosigmoid Approach: 3-Dimensional Operative Video.
Operative neurosurgery (Hagerstown, Md.), 2019

A 22-yr-old female college athlete had noted ataxia during competitive gymnastic events. Magnetic resonance imaging revealed a large tumor compatible with preoperative diagnosis of meningioma arising from the petrotentorial region with marked brainstem compression. The technical challenges associated with this removal include safe dissection of cranial nerves IV to VIII and dissection from the brainstem and cerebellum, taking care to not interfere with blood supply to these structures. The vascular tumor was removed via standard suboccipital approach, with the trajectory above the seventh/eighth nerve complex. The attachment was at the petrotentorial junction, and the fourth nerve was intimately involved with the tumor as the tumor was emanating from the tentorial edge where the fourth nerve entered. In most instances, the nerves are displaced by the tumor but in this case injury to the fourth nerve ensued with dissection at the tumor attachment. After tumor resection, the interrupted fourth nerve was repaired microsurgically. A hemangiopericytoma was identified on pathological analysis, and the patient received postoperative radiation therapy, which has been given postoperatively or at recurrence in the literature. Technical nuances of removal are discussed. Patient consent was granted for publication of this video.
Structure and function of cerebral and mesenteric resistance arteries in low-dose endotoxin-infused pregnant rats.
Pregnancy hypertension, 2013

Since the cerebrovasculature likely plays a prominent role in the pathophysiology of eclampsia, we assessed the effects of low-dose endotoxin-induced experimental preeclampsia on the function and structure of rat posterior cerebral arteries (PCA) and mesenteric arteries (MA).
[Neurophysiology in Guillain-Barré syndrome].
Brain and nerve = Shinkei kenkyu no shinpo, 2015

The electrodiagnostic features for the demyelinating and axonal subtypes of Guillain-Barré syndrome (GBS) were described. In the early stage of demyelinating GBS, the most prominent neurophysiologic feature is the patchy demyelination in the peripheral nerves. Conduction slowing presents in the clinical recovery stage, which indicates the conduction slowing is due to mainly remyelination. Axonal GBS shows "reversible conduction failure", as well as primary axonal degeneration. "Reversible conduction failure" is thought to be the most common cause of the underestimation of axonal GBS. The electrodiagnostic criteria for GBS subtypes should be revised based on the knowledge acquired in recent years.
Subunit-Specific Augmentation of AMPA Receptor Ubiquitination by Phorbol Ester.
Cellular and molecular neurobiology, 2020

Excitatory neurotransmission relies on the precise targeting of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors to the neuronal plasma membrane. Activity-dependent ubiquitination of AMPA receptor (AMPAR) subunits sorts internalised receptors to late endosomes for degradation, which ultimately determines the number of AMPARs on neuronal membrane. Our recent study has demonstrated a functional cross-talk between the phosphorylation and ubiquitination of the GluA1 subunit in mammalian central neurons. However, the existence of such a cross modulation for the GluA2 subunit remains unknown. Here, we have shown that bicuculline induced GluA2 ubiquitination on the same lysine residues (Lys-870 and Lys-882) in the C-terminal as those elicited by the AMPA treatment. Interestingly, bicuculline-induced ubiquitination was markedly enhanced by the phospho-mimetic GluA2 S880E mutant. Pharmacological activation of protein kinase C (PKC) by phorbol ester, which mediates the phosphorylation of GluA2 at Ser-880, augmented bicuculline-induced ubiquitination of GluA2 in cultured neurons. This effect was specific for the GluA2 subunit because phorbol ester did not alter the level of GluA1 ubiquitination. However, phorbol ester-induced enhancement of GluA2 ubiquitination did not require Ser-880 phosphorylation. This suggests that pseudo-phosphorylation of Ser-880 is sufficient but is not necessary for the augmentation of bicuculline-induced GluA2 ubiquitination. Collectively, these data provide the first demonstration of subunit-specific modulation of AMPAR ubiquitination by the PKC-dependent signalling pathway in mammalian central neurons.
Emerging Therapeutic Promise of Ketogenic Diet to Attenuate Neuropathological Alterations in Alzheimer's Disease.
Molecular neurobiology, 2020

Alzheimer's disease (AD) is a multifactorial and chronic neurodegenerative disorder that interferes with memory, thinking, and behavior. The consumption of dietary fat has been considered a vital factor for AD as this disease is related to blood-brain barrier function and cholesterol signaling. The ε4 allele of apolipoprotein E (APOE4) is a primary genetic risk factor that encodes one of many proteins accountable for the transport of cholesterol and it is deemed as the leading cholesterol transport proteins in the brain. In case of AD development, the causative factor is the high level of serum/plasma cholesterol. However, this statement is arguable and, in the meantime, the levels of brain cholesterol in individuals with AD are extremely inconstant and levels of cholesterol in the brain and serum/plasma of AD individuals do not reflect cholesterol as a risk factor. In fact, APOE4 is neither fundamental nor sufficient for the advancement of AD; it just acts as a synergistic and increases the danger of AD. Another noticeable characteristic of AD is area-specific decreases in the metabolism of brain glucose. It has been found that the brain cells cannot efficiently metabolize fats; hence, they totally rely upon glucose as a vitality substrate. Thus, suppression of glucose metabolism can possess an intense effect on brain actions. Hypometabolism is frequently found in AD and has quite recently achieved impressive consideration as a plausible target for interfering in the progression of the disease. One promising approach is to keep up the normal supply of glucose to the brain with ketone bodies from the ketogenic diet signifies a potential therapeutic agent for AD. Therefore, this review represents the role of ketogenic diets to combat AD pathogenesis by considering the influence of APOE.
Impaired lipid metabolism in astrocytes underlies degeneration of cortical projection neurons in hereditary spastic paraplegia.
Acta neuropathologica communications, 2020

Hereditary spastic paraplegias (HSPs) are caused by a length-dependent axonopathy of long corticospinal neurons, but how axons of these cortical projection neurons (PNs) degenerate remains elusive. We generated isogenic human pluripotent stem cell (hPSC) lines for two ATL1 missense mutations associated with SPG3A, the most common early-onset autosomal dominant HSP. In hPSC-derived cortical PNs, ATL1 mutations resulted in reduced axonal outgrowth, impaired axonal transport, and accumulated axonal swellings, recapitulating disease-specific phenotypes. Importantly, ATL1 mutations dysregulated proteolipid gene expression, reduced lipid droplet size in astrocytes, and unexpectedly disrupted cholesterol transfer from glia to neurons, leading to cholesterol deficiency in SPG3A cortical PNs. Applying cholesterol or conditioned medium from control astrocytes, a major source of cholesterol in the brain, rescued aberrant axonal transport and swellings in SPG3A cortical PNs. Furthermore, treatment with the NR1H2 agonist GW3965 corrected lipid droplet defects in SPG3A astrocytes and promoted cholesterol efflux from astrocytes, leading to restoration of cholesterol levels and rescue of axonal degeneration in SPG3A cortical PNs. These results reveal a non-cell autonomous mechanism underlying axonal degeneration of cortical PNs mediated by impaired cholesterol homeostasis in glia.
Functional analysis of information rates conveyed by rat whisker-related trigeminal nuclei neurons.
Journal of neurophysiology, 2021

The rat whisker system connects the tactile environment with the somatosensory thalamocortical system using only two synaptic stages. Encoding properties of the first stage, the primary afferents with somas in the trigeminal ganglion (TG), has been well studied, whereas much less is known from the second stage, the brainstem trigeminal nuclei (TN). The TN are a computational hub giving rise to parallel ascending tactile pathways and receiving feedback from many brain sites. We asked the question, whether encoding properties of TG neurons are kept by two trigeminal nuclei, the principalis (Pr5) and the spinalis interpolaris (Sp5i), respectively giving rise to two "lemniscal" and two "nonlemniscal" pathways. Single units were recorded in anesthetized rats while a single whisker was deflected on a band-limited white noise trajectory. Using information theoretic methods and spike-triggered mixture models (STM), we found that both nuclei encode the stimulus locally in time, i.e., stimulus features more than 10 ms in the past do not significantly influence spike generation. They further encode stimulus kinematics in multiple, distinct response fields, indicating encoding characteristics beyond previously described directional responses. Compared with TG, Pr5 and Sp5i gave rise to lower spike and information rates, but information rate per spike was on par with TG. Importantly, both brainstem nuclei were found to largely keep encoding properties of primary afferents, i.e. local encoding and kinematic response fields. The preservation of encoding properties in channels assumed to serve different functions seems surprising. We discuss the possibility that it might reflect specific constraints of frictional whisker contact with object surfaces.