bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation between the health of individuals directly affected by the COVID‐19 pandemic and dementia
Authors: Khanna Deepesh , Patel Nishant 
Published: December 2023

AbstractBackgroundThis qualitative literature review analyzed the correlation between the health of individuals directly affected by the COVID‐19 pandemic and dementia.MethodWe used EndNote 20 to acquire our sources, where PubMed was the main source of data collection. Search inquiries included “COVID‐19”, “dementia”, “Alzheimer’s” and “demyelination”. A total of 25 studies were published between 2020 and 2022, out of which 13 studies were analyzed. Each publication provides details about the impact of COVID‐19 on either patient with pre‐existing dementia, or its onset due to the side effects caused by vaccination, such as demyelination. Changes were measured by utilizing the NPI scale and recognizing changes to behavioral and psychological symptoms (BPSD).ResultNot only did the severity of dementia increase with age in the studies observed, but symptoms also increased when shifting to a total lockdown environment. Moreover, patients with increased severity of the SARS‐CoV‐2 infection are associated with an increased risk of developing progressive dementia and Alzheimer’s. The data collected through our literature search presents anticipated findings with previously published literature providing a correlation between COVID‐19 and neuropsychiatric diseases. Overall, the compiled results indicate an increase in anxiety, depression, and apathy levels among patients, insinuating a correlation between COVID‐19 and its impact on progressive dementia. Limitations of this study include the specificity of the subject. As the outbreak is still relatively recent, long‐term implications of the SARS‐CoV‐2 virus are unprecedented and there is limited literature on this topic.ConclusionThe findings of our study strengthen previously published literature on the psychological impacts of COVID‐19. The importance of this field sheds light on a need for further studies providing data on the long‐term implications between the variables of COVID‐19 and dementia, to provide concrete medical care and prevention methods for future pandemics synonymous with the COVID‐19 pandemic.References1.Cinar, N., et al. (2022). “Neuropsychiatric Effects of COVID‐19 Pandemic on Alzheimer’s Disease: A Comparative Study of Total and Partial Lockdown.” Sisli Etfal Hastan Tip Bul 56(4): 453‐460.2. Delgado‐Alonso, C., et al. (2022). “Cognitive dysfunction associated with COVID‐19: A comprehensive neuropsychological study.” J Psychiatr Res 150: 40‐46.
Hippocampal function during an associative memory task is influenced by early bilateral salpingo‐oophorectomy
Authors: Brown Alana , Gravelsins Laura , Gervais Nicole J , Rieck Jenny , Almey Anne , Reuben Rebekah , Karkaby Laurice , Zhao Sophia , Rusu Simone , Duchesne Annie , Witt Suzanne Tyson , Kämpe Robin , Classon Elisabet , Lykke Nina , Theodorsson Elvar , Ernerudh Jan , Lundqvist Elisabeth Åvall , Kjølhede Preben , Engström Maria , Grady Cheryl , Einstein Gillian 
Published: December 2023

AbstractBackgroundWomen with mid‐life 17β‐estradiol loss due to early bilateral salpingo‐oophorectomy (BSO; removal of ovaries and fallopian tubes) have heightened Alzheimer’s disease (AD) risk (Rocca et al., 2007). 17β‐estradiol loss is related to AD risk factors, including associative memory decrements and decreased functional magnetic resonance imaging (fMRI)‐measured hippocampal activation during encoding (Jacobs et al., 2016; Rentz et al., 2017). Our objective was to investigate the effects of early BSO and 17β‐estradiol replacement therapy (ERT) on associative memory and hippocampal function.MethodWomen with BSO either taking ERT (BSO+ERT; M±SEage= 45±1.03, n = 23) or not taking ERT (BSO; M±SEage= 45.7±1.01, n = 23) were compared to age‐matched premenopausal control women (AMC; M±SEage= 43.7±0.48, n = 37) on fMRI‐measured brain activation during encoding and retrieval trials of a face‐name associative memory task. We compared groups on activation from anterior and posterior anatomical hippocampal regions‐of‐interest during retrieval and encoding (retrieval‐encoding contrast) trials between groups. We also compared hippocampal activation during novel and repeat face‐name pair encoding trials (novel‐repeat encoding contrast). Face‐name pair recognition accuracy between groups was also assessed.ResultCompared to BSO+ERT, BSO exhibited significantly lower activation during novel compared to repeat encoding trials (Fig.1A) in the right anterior hippocampal region‐of‐interest (Fig.1B). There were no significant group differences in hippocampal activation during retrieval compared to encoding trials, and no group differences in recognition accuracy.ConclusionYounger women with BSO either taking ERT or not showed comparable hippocampal activation to age‐matched premenopausal women during retrieval of face‐name pairs. However, during encoding of face‐name pairs, BSO showed significantly lower right anterior hippocampal activation compared to BSO+ERT. ERT may influence associative encoding processes dependent on hippocampal novelty detection, rather than retrieval processes. Expanding on work from others (Phillips & Sherwin, 1992), these results suggest ERT may ameliorate the negative influence of oophorectomy on hippocampal‐dependent memory processes.
Translation and adaptation of a questionnaire for assessing cognitive domains based on the diagnostic criteria of the Diagnostic and Statistical Manual of Mental Disorders ‐ DSM‐5 for neurocognitive disorders
Authors: Diniz Maissa Ferreira , Ferreira Jéssica Diniz , Souza Nicolau Mariana , Diniz Breno Satler , Romano‐Silva Marco Aurélio , Malloy‐Diniz Leandro F , Bicalho Maria Aparecida Camargos , de Paula Jonas Jardim , Mattos Viana Bernardo 
Published: December 2023

AbstractBackgroundThe Cognitive Domains and Functional Assessment Questionnaire (QACDF) assesses cognitive and functional decline based on the DSM‐5 criteria for Neurocognitive Disorders¹. The QACDF has two versions, one for the patient and another for the informant. It is composed of 30 items, each assessed by a likert scale. This questionnaire has appropriate semantic characteristics for the Brazilian older adult population.MethodThe objective of this study was to translate, adapt and assess the semantic, idiomatic, experiential and conceptual equivalence of the QACDF. Firstly, the QADCF original version in Portuguese was translated to English by two Bilingual translators, a non‐specialist linguist and a specialist in the field. After this, the two translators (T1 and T2) together with a mediator translator synthesized the translations in a common version (T3). Then, the T3 version was back‐translated into Portuguese by a Bilingual translator, blind to the original version². The three versions (original, translated and back‐translated) were assessed by a committee of specialists. The committee was composed of the initial translators, an English native speaker, an expert in the methodology and the main researchers.ResultThe QACDF Items were adjusted to conceive equivalent expressions for the target language, as well as to assess cognitive domains and the functionality of daily living of English speakers. Semantic, idiomatic, experiential and conceptual equivalence were debated by the committee until consensus was reached.ConclusionThe translation of the instrument followed the proposed methodology by Beaton et col. However, while the Brazilian Portuguese versions have been assessed by two pilot studies, pilot studies are still needed to further adjust the questionnaires for English speakers.
Neuroprotective potential of carbamide forte on LPS‐induced experimental PD
Authors: Ranjan Suray , Sharma Priyanka , Deshmukh Rahul Renukadas 
Published: December 2023

AbstractBackgroundParkinson’s disease is a second most common age‐related neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta region of the midbrain. Increased oxidative stress and inflammation with decreased activity of glutathione peroxidase, superoxide dismutase (SOD), and catalase has been observed in PD patients. Carbamide Forte Brain and Memory Support is blend of 9 herbal brain‐enhancing ingredients to boost short term cognitive function and long‐term brain health and thus expected to be beneficial in cognition and movement disorder.MethodAdult male/female Sprague Dawley rats were ICV injected with LPS at a dose of 0.2 mg/kg body weight into substantia nigra pars compacta with the help of stereotaxic apparatus. Carbamide Forte was administered per orally at 80 and 160 mg/kg body weight, 4 days after to LPS infusion.ResultInfusion of single ICV‐LPS produced significantly decreased in body weight, locomotor activity, motor coordination, antioxidant defense enzymes and significantly increased oxidative stress markers in the striatum. Chronic administration of carbamide forte (for 21days) significantly attenuated LPS induced movement disabilities in Narrow beam walk, Horizontal ladder beam walk test, OFT and also significantly reduce the oxidative‐nitrosative stress and antioxidants enzymesas evidence by decrease in malondialdehyde and nitrite levels and restored the reduced glutathione level in rats & neuroprotective potential of CF with morphological changes seen in our histological assessment. The observed result of the present study is indicative of the therapeutic potential of Carbamide Forte in PD.ConclusionIt could be concluded that the observed neuroprotective effect of Carbamide Forte may be due to antioxidant and neuroprotective potential.
β‐Asarone attenuates streptozotocin‐induced experimental dementia in rats: Possible role of phosphodiesterases and cyclic nucleotide signaling
Authors: Kumar Narinder , Kumar Ashwani , Deshmukh Rahul Renukadas 
Published: December 2023

AbstractBackgroundIn recent years, extract of Acorus calamus shown to inhibit phosphodiesterases (PDE) and β‐asarone has been reported to be a major active constituent. The purpose of the present study was to ascertain PDE inhibitory potential of β‐asarone and to explore its therapeutic potential in sporadic Alzheimer’s type dementia (SAD). In the current study, PDE inhibitory potential of β‐asarone was determined using in vitro assay system.MethodStreptozotocin (STZ) was infused intracerebroventrically [bilaterally (3 mg/kg) ICV] to induce SAD in rats. Spatial and non‐spatial memory was evaluated using Morris water maze and object recognition task in rats.Rats were treated with β‐asarone (12.5, 25 and 50 mg/kg) from day 10 to 21 following 1st STZ infusion. On day 22 rats were sacrificed and the cortical and hippocampal brain regions were used to identify biochemical alterationsResultSTZ infused rats showed significant learning and memory deficit which was linked with increase in oxidative stress (malondialdehyde and nitrite), compromised antioxidant defense (reduced glutathione), mitochondrial dysfunction (deficit in complex I and III activity) and pro‐inflammatory cytokine levels. Significant decrease in both cAMP and cGMP levels were also observed in STZ‐infused rats. β‐Asarone dose dependently attenuated STZ‐induced cognitive deficit, biochemical alterations and restored cyclic nucleotide levels.ConclusionThe observed results show important role of PDE inhibition and cyclic nucleotide signaling in the beneficial effects of β‐asarone and suggest therapeutic potential of β‐asarone in the management of cognitive disorders.
Self‐reported COVID‐19 and biomarkers of Alzheimer’s disease: interim analyses from an Alzheimer’s disease risk‐enriched cohort
Authors: Akinci Muge , Shekari Mahnaz , Palpatzis Eleni , González Escalante Armand , Contador Israel , Argiris Georgette , Fuentes‐Julian Sherezade , Kollmorgen Gwendlyn , Carboni Margherita , Blennow Kaj , Zetterberg Henrik , Minguillon Carolina , Fauria Karine , Knezevic Iva , Navarro Arcadi , Sánchez‐Benavides Gonzalo , Grau‐Rivera Oriol , Suarez‐Calvet Marc , Gispert Juan Domingo , Arenaza‐Urquijo Eider M 
Published: December 2023

AbstractBackgroundCOVID‐19‐related SARS‐CoV‐2 infection has been linked with brain abnormalities and cerebrospinal fluid (CSF) biomarkers of Alzheimer’s disease (AD), neuroinflammation, and neuronal injury. Whether COVID‐19 increases the brain’s vulnerability to the development of AD is unclear. In participants at an increased risk of AD, we investigated the association of COVID‐19 with pre‐ and post‐pandemic AD biomarkers.MethodWe included 132 cognitively unimpaired adults from the ALFA+ cohort (52‐71 years, 61.4% women) who provided retrospective self‐reported data on SARS‐CoV‐2 infection (with COVID‐19 vs. without COVID‐19). As of February 2022, 125 (94.7%) participants had available CSF biomarkers (measured with exploratory Roche NeuroToolKit or Elecsys® immunoassays, Roche Diagnostics International Ltd, Rotkreuz, Switzerland) and 76 (57.6%) had [18F]flutemetamol‐PET data acquired before (pre‐pandemic) and after (post‐pandemic) the beginning of the COVID‐19 pandemic (average time lapse between the assessments: 3.5±0.6 years). [18F]flutemetamol PET SUVR maps were obtained using the whole cerebellum as the reference region. First, we performed ANCOVA models to investigate whether COVID‐19 was associated with post‐pandemic CSF biomarkers of core AD pathology (Aβ42/40 and p‐tau), neuronal injury (NfL), and neuroinflammation (sTREM2, GFAP, and IL‐6), while controlling for pre‐pandemic biomarker levels. Covariates were age, sex, years of education, APOE‐ε4 status, and time lapse between the biomarker assessments. Second, we performed a voxel‐wise analysis in SPM‐12 using a matched‐group comparison design (with COVID‐19 vs. without COVID‐19 matched by pre‐pandemic Centiloid values, age, and APOE‐ε4 status) with the post‐pandemic amyloid‐PET scans as the outcome of interest.ResultFifteen (12%) participants included in ANCOVA reported COVID‐19. Eleven (14.5%) with amyloid‐PET scans reported COVID‐19 and were matched with 11 participants without COVID‐19 for voxel‐wise analysis. In ANCOVA models, no significant association between COVID‐19 and post‐pandemic CSF biomarkers was found (Table 1). Results from the t‐test voxel‐wise analysis also did not show any differences between participants with vs. without COVID‐19 on [18F]flutemetamol‐PET uptake after correction with false discovery rate.ConclusionOur interim analyses did not show any association between self‐reported COVID‐19 and post‐pandemic biomarkers of AD pathology, neuronal injury, and neuroinflammation. The results are pending confirmation of COVID‐19 status using serology data (n = 181) and complete sample size.
Neurophysiological alterations in mice and humans carrying mutations in APP and PSEN1 genes
Authors: van Heusden Fran C , van Nifterick Anne M , Souza Bryan C. , França Arthur S.C. , Stam Cornelis J , Scheltens Philip , Smit August B. , Gouw Alida A , van Kesteren Ronald E. 
Published: December 2023

AbstractBackgroundStudies in animal models of Alzheimer’s disease (AD) have provided valuable insights into the molecular and cellular processes underlying neuronal network dysfunction, but whether and how AD‐related neurophysiological alterations translate between mice and men remains uncertain.MethodWe characterized neurophysiological alterations in mice and humans carrying AD mutations in the APP and/or PSEN1 genes, focusing on early changes. Longitudinal local field potential recordings were peformed in 3‐12‐month‐old APP/PS1 mice and cross‐sectional magnetoencephalography recordings in pre‐symptomatic human APP and PSEN1 mutation carriers. Recordings were acquired of the left hippocampus, frontal and parietal cortex. We performed spectral activity and functional connectivity analyses and results were compared with wildtype control mice and healthy age‐matched human subjects.ResultAPP/PS1 mice showed increased aboslute power, especially at higher frequencies (beta and gamma) and predominantly between 3 and 6 months of age. Relative power showed an overall shift from lower to higher fequencies over almost the entire recording period and across all three brain regions. There was a trend for reduced peak frequency in APP/PS1 mice at 3‐4 months of age. Human mutation carriers did not show changes in power except for an increase in relative theta power in the hippocampus. Parietal cortex and hippocampal peak frequency were reduced in human mutation carriers. In both models, significant alteration in functional connectivity were detected in theta, alpha, beta and gamma frequency bands, but the exact frequency range and direction of change differed for APP/PS1 mice and human mutation carriers (Table 1).ConclusionIn conclusion, both mice and humans carrying APP and/or PSEN1 mutations show abnormal neurophysiological activity, but several measures do not translate one‐to‐one between species. Alterations in spectral characteristics and functional connectivity in mice should be interpreted with care and may be due to overexpression of amyloid in combination with absence of tau pathology in cholinergic degeneration. Future studies should explore whether changes in brain activity in other AD mouse models provide better translation to the human AD continuum.
Early Detection of Alzheimer’s Disease using microRNAs
Authors: Heuvelman Marco , Horos Rastislav , Sikosek Tobias , Tikk Kaja , Rajakumar Timothy , Cummings Jeffrey L. , Hansen Niels , Bartels Claudia , Oberstein Timo Jan , Hausner Lucrezia , Wiltfang Jens , Frölich Lutz , Steinkraus Bruno R 
Published: December 2023

AbstractBackgroundMicroRNAs (miRNAs) represent a class of ∼22nt short non‐coding RNAs that have been identified as a sophisticated layer of post‐transcriptional regulation, governing many cellular, inflammatory and vascular processes. Their biological importance, together with the observation that miRNAs are frequently secreted into the extracellular space and stable in blood serum/plasma and other body fluids, make them specific, robust and non‐invasive biomarkers that could augment the amyloid and tau framework. miRNAs have been used for the detection of prodromal and early Alzheimer’s disease (AD) (e.g., mild cognitive impairment (MCI) due to AD) and to improve the differential diagnosis of AD. However, to date no miRNA panel has been translated into a clinical test.MethodIn collaboration with the University of Göttingen, the University of Erlangen and Zentralinstitut für Seelische Gesundheit in Mannheim, we prospectively collected PAXgene whole blood from 225 individuals (55‐85 years of age, MMSE ≥20) phenotyped at the respective memory clinics according to state‐of‐the‐art AD diagnostics including CSF core biomarkers. Amyloid positivity as a well validated proxy of brain β‐amyloidosis was determined using a CSF ABeta42/ABeta40 threshold of 0.075. Thus, 127 individuals were ABeta(+) and 96 individuals were ABeta(‐). We deployed 100‐fold cross validation of a linear regression classifier to construct and validate small RNA feature models to evaluate their utility as biomarkers for amyloid positivity and AD diagnosis.ResultWe generated small RNA feature models and report a median diagnostic receiver operating area under the curve (AUC) of 0.66 (95% CI 0.59‐0.76) for amyloid positivity (ABeta42/ABeta40 < 0.075). We deconvolved our whole blood sRNA signature into their respective plasma or immune cell origin. We found that the predicting features largely originate from the plasma fraction of whole blood (48.8%), marking a significant increase over the unselected distribution of all features (13.1%) of 3.72‐fold (p<0.001). However, several predictive features were found to originate from peripheral immune cells, particularly of the lymphoid arm (CD4+, CD8+ and B‐cells).ConclusionThese data suggest the potential of a small RNA‐based blood test as a viable complement to the AT(N) framework for the management of individuals at risk for AD.
Sleep fragmentation affects glymphatic system through the different expression of AQP4 in wild type and 5xFAD mouse models
Authors: Vasciaveo Valeria , Iadarola Antonella , Casile Antonino , Morello Giulia , Dante Davide , Minotta Lorenzo , Tamagno Elena , Cicolin Alessandro , Guglielmotto Michela 
Published: December 2023

AbstractBackgroundSleep is an important physiological process, during which extracellular metabolic wastes, such as amyloid and tau protein, are cleared via paravascular pathway. Changes in the timing and structure of sleep occur across the lifespan. Increased sleep fragmentation and reductions in slow wave sleep (SWS) represent the hallmark signs of age‐related changes in sleep. The origin of sleep disturbances in AD is thought to be multifactorial. In the aging brain, the impairment of glymphatic pathway function slows the clearance of interstitial Aβ, rendering the aging brain vulnerable to neurodegenerative disease. Several authors have independently shown that glymphatic flux depends upon the expression and perivascular localization of the astroglial water channel aquaporin‐4 (AQP4).MethodIn this study, we performed and validated a mouse model of AD and chronic sleep fragmentation, a sleep disorder that mimics more correctly a real condition of intermittent and continuous awakening. We analyzed the effect of sleep fragmentation in wild type and 5xFAD mice. All the animals underwent to behavioral studies to analyze anxiety and spatial and working memory. We had validated sleep fragmentation and its effect through EEG and biomolecular analysis, by observing all the macro‐areas implied in sleep regulation.ResultWe noticed that sleep fragmentation induces a general acceleration of AD progression in 5xFAD mice, while in wild type mice it affects cognitive behaviors in particular learning and memory. Both these events may be correlated to AQP4 modulation, a crucial player of the glymphatic system activity. In particular, sleep fragmentation differentially affects AQP4 expression according to the stage of the disease, with an up‐regulation in younger animals, while such change cannot be detected in older ones. Moreover, in wild type mice sleep fragmentation affects cognitive behaviors, in particular learning and memory, by compromising the glymphatic system through the decrease of AQP4.ConclusionNevertheless, an in‐depth study is needed to better understand the mechanism by which AQP4 is modulated and whether it could be considered a risk factor for the disease development in wild type mice. If our hypotheses are going to be confirmed, AQP4 modulation may represent the convergence point between AD and sleep disorder pathogenic mechanisms