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423
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ShareScore release 0.9.0
Dataset results
423 results for “Brain aging”
Brain Imaging Biomarkers of Pathological Brain Aging in Late-life Depression
ClinicalTrials.gov study NCT03849417. IPD Sharing: UNDECIDED. Countries: 1. Publications: 2.
Measuring Brain Activity of School Age Children
ClinicalTrials.gov study NCT03407729. IPD Sharing: UNDECIDED. Countries: 1. Publications: 20.
Brain–muscle tissue communication prevents muscle aging by maintaining daily physiology
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Gut dysbiosis and brain microhemorrhages in young vs aged mice with chronic kidney disease
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A 3D Adult Zebrafish Brain Atlas (AZBA) for the Digital Age
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Data from: Effects of maternal age and environmental enrichment on learning ability and brain size
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Whole-transcriptome sequencing identifies neuroinflammation, metabolism and blood-brain barrier related processes in the hippocampus of aged mice during perioperative period
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Data from: Sleep, inflammation, and cognitive behavior of aged wild-type mice subjected to diffuse brain injury and aged 3xTg-AD mice as a model of Alzheimer’s disease
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Data from: Cognition at age 70: life course predictors and associations with brain pathologies
Objective: To investigate predictors of performance on a range of cognitive measures including the Preclinical Alzheimer Cognitive Composite (PACC) and test for associations between cognition and dementia biomarkers in Insight 46, a sub-study of the MRC National Survey of Health and Development. Methods: 502 individuals born in the same week in 1946 underwent cognitive assessment at age 69-71 years, including an adapted version of the PACC and a test of non-verbal reasoning. Performance was characterised with respect to sex, childhood cognitive ability, education and socioeconomic position (SEP). In a sub-sample of 406 cognitively-normal participants, associations were investigated between cognition and β-amyloid (Aβ) positivity (determined from Aβ-PET imaging), whole brain volumes, white matter hyperintensity volumes (WMHV), and APOE-ε4. Results: Childhood cognitive ability was strongly associated with cognitive scores including the PACC more than 60 years later, and there were independent effects of education and SEP. Sex differences were observed on every PACC sub-test. In cognitively-normal participants, Aβ-positivity and WMHV were independently associated with lower PACC scores, and Aβ-positivity was associated with poorer non-verbal reasoning. Aβ-positivity and WMHV were not associated with sex, childhood cognitive ability, education or SEP. Normative data for 339 cognitively-normal Aβ-negative participants are provided. Conclusions: This study adds to emerging evidence that subtle cognitive differences associated with Aβ deposition are detectable in older adults, at an age when dementia prevalence is very low. The independent associations of childhood cognitive ability, education and SEP with cognitive performance aged 70 have implications for interpretation of cognitive data in later life.
Data from: Circulating cortisol and cognitive and structural brain measures in a middle-aged cohort: the Framingham Heart Study
Objective: To assess the association of early morning serum cortisol with cognitive performance and brain structural integrity in community-dwelling young and middle-aged adults without dementia. Methods: We evaluated dementia-free Framingham Study (Generation 3) participants (mean age 48.5 years; 46.8% men), who underwent cognitive testing for memory, abstract reasoning, visual perception, attention, and executive function (n= 2231), and brain MRI (n=2018) to assess total white matter, lobar gray matter, and white matter hyperintensity volumes and fractional anisotropy (FA) measures. We used linear and logistic regression to assess the relations of cortisol (categorized in tertiles, with the middle tertile as referent) to measures of cognition, MRI volumes, presence of covert brain infarcts (CBI) and cerebral microbleeds (CMB), and voxel-based microstructural white matter integrity and gray matter density, adjusting for age, sex, APOE and vascular risk factors. Results: Higher cortisol (highest tertile vs. middle tertile) was associated with worse memory and visual perception, as well as lower total cerebral brain, occipital and frontal lobar gray matter volumes. Higher cortisol was associated with multiple areas of microstructural changes (decreased regional FA), especially in the splenium of corpus callosum and the posterior corona radiata. The association of cortisol with total cerebral brain volume varied by sex (p interaction=0.048); higher cortisol was inversely associated with cerebral brain volume in women [p=0.001] but not in men [p=0.717]). There was no effect modification by the apoE4 genotype of the relations of cortisol and cognition or imaging traits. Conclusions: Higher serum cortisol was associated with lower brain volumes and impaired memory in asymptomatic younger to middle-aged adults, with the association being evident particularly in women.
Supplementary Data to: Mediterranean diet, Alzheimer's disease biomarkers and brain atrophy in old age
<p><b>Objective:</b> To determine if following a Mediterranean-like diet (MeDi) relates to cognitive functions and <i>in vivo</i> biomarkers for Alzheimer's disease (AD), we analyzed cross-sectional data from the German Longitudinal Cognitive Impairment and Dementia Study</p> <p><b>Method:</b> The sample (n=512, mean age: 69.5±5<span>.9 years) </span><span><span>included 169 cognitively normal participants and subjects at higher AD risk (53 AD relatives, 209 SCD and 81 MCI).</span></span><span> We </span>defined MeDi adherence based on the Food Frequency Questionnaire. Brain volume outcomes were generated via voxel-based morphometry on T1-MRI and cognitive performance with an extensive neuropsychological battery. AD-related biomarkers (Aβ42/40 ratio, pTau181) in cerebrospinal fluid were assessed in n=226 individuals. We analyzed the associations between MeDi and the outcomes with linear regression models controlling for several covariates. Additionally, we applied hypothesis-driven mediation and moderation analysis. </p> <p><b>Results:</b> Higher MeDi adherence related to larger mediotemporal gray matter volume (p<0.05 FWE corrected), better memory (β±SE = 0.03 ± 0.02; p=0.038), and less amyloid (Aβ42/40 ratio, β±SE = 0.003 ± 0.001; p=0.008) and pTau181 pathology (β±SE = -1.96±0.68; p=0.004). Results were consistent correcting for ApoE- ε4 status. Mediotemporal volume mediated the association between MeDi and memory (40% indirect mediation). Finally, MeDi favorably moderated the associations between Aβ42/40 ratio, pTau181 and mediotemporal atrophy. </p> <p><b>Conclusion:</b> Our findings corroborate the view of MeDi as a protective factor against memory decline and mediotemporal atrophy. Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. Longitudinal and dietary intervention studies should further examine this conjecture and its treatment implications.</p>
Data from: Age-at-injury influences the glial response to traumatic brain injury in the cortex of male juvenile rats
<p>Glia influence neuronal development and aging. Few translational studies have examined how age at injury affects the glial response to traumatic brain injury (TBI). We hypothesized that rats injured before sexual maturity would exhibit a greater glial response, that persists into early adulthood, compared to rats injured near the onset of sexual maturity.</p> <p>Postnatal day (PND)17 and PND35 rats received midline fluid percussion injury or sham surgery. In three cortical regions (peri-injury, S1BF, perirhinal), we investigated the glial response relative to age at injury, time post-injury (2H, 1D 7D, 25D, and 43D), and post-natal age, such that rats injured at PND17 or PND35 were compared at the same post-natal-age (e.g., PND17+25d post-injury=PND42; PND35+7d post-injury=PND42). We measured Iba1+ microglia cells and quantified their activation status. GFAP expression was examined using immunohistochemistry. Data were analyzed using Bayesian multivariate multi-level models.</p> <p>Independent of age at injury, TBI activated microglia (shorter branches, fewer endpoints) in the cortex with more microglia in all regions compared to shams. TBI-induced microglial activation was sustained in the S1BF into early adulthood (PND60). PND17 injured rats had more microglial activation in the perirhinal cortex than PND35 injured rats. Activation was not confounded by age-dependent cell size changes, and microglial cell body sizes were similar between ages.</p> <p>Increased microglial activation in PND17 injured rats suggests that TBI upregulates the glial response at discrete stages of development. Age at injury and aging with an injury are translationally important because experiencing a TBI during early childhood may trigger an exaggerated glial response.</p>
Processed MERFISH datasets for brain aging (coronal, sagittal) and rejuvenation (exercise, partial reprogramming)
<p>This repository contains several AnnData ".h5ad" objects containing the processed MERFISH data and metadata for the datasets generated in our study:</p> <blockquote> <p>"aging_coronal.h5ad" - the aging coronal section dataset</p> <p>"aging_sagittal.h5ad" - the aging sagittal section dataset</p> <p>"exercise.h5ad" - exercise dataset</p> <p>"reprogramming.h5ad" - partial reprogramming dataset</p> </blockquote> <p> </p> <p>Key metadata are saved as observation annotations in each object, and include:</p> <blockquote> <p>"mouse_id" - identifier for mouse from which the cell was derived</p> <p>"slide_id" - identifier for MERSCOPE slide</p> <p>"batch" - A and B denote different experimental batches for MERFISH</p> <p>"age" - mouse age in months</p> <p>"cohort" - experimental condition / group</p> <p>"celltype" - cell type annotation</p> <p>"region" - brain region annotation</p> <p>"subregion" - brain subregion annotation (will be more variabile/noisy than region)</p> </blockquote>
Processed Data for Cell type-specific aging clocks to quantify aging and rejuvenation in regenerative regions of the brain
<p>Seurat objects for data accompanying the publication "Cell type-specific aging clocks to quantify aging and rejuvenation in regenerative regions of the brain".</p> <p>Preprint available at <a href="https://doi.org/10.1101/2022.01.10.475747">https://doi.org/10.1101/2022.01.10.475747</a></p> <ul> <li>multi_intergrated_seurat_Dec2020.rds is the data from the SVZ of the cohort of 28 mice across different ages</li> <li>pb_combined.rds is the data from the SVZ of both heterochronic parabiosis mouse cohorts</li> <li>Dulken_svz_celltypes_2019-01-31.rda is the data associated with <a href="https://doi.org/10.1038/s41586-019-1362-5">https://doi.org/10.1038/s41586-019-1362-5</a></li> </ul> <p> </p>
Paired blood-brain transcriptomes (GTEx v8), age and sex preserved
<p>This dataset includes pre-normalized paired blood-brain RNA-sequencing profiles from donors included in the Genotype Tissue Expression (GTEx) Project (v8). Variances in gene expression associated with age and sex were preserved during normalization. These data are formatted for BrainGENIE. </p>
Milk Intervention Study for Brain Aging
ClinicalTrials.gov study NCT02957422. IPD Sharing: NO. Countries: 1. Publications: 1.
tDCS Effects on GABA Concentration and Brain Functional Connectivity in Older Adults of Retirement Age
ClinicalTrials.gov study NCT02794259. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Spatial and Dynamic Characterization of Brain Activity for Language and Posture (Verticality) During Normal Aging. Magnetoencephalography (MEG) Study (MEG-AGING)
ClinicalTrials.gov study NCT04036162. IPD Sharing: Not stated. Countries: 1. Publications: 3.
The Brain Mechanism of Social Emotion and Communication in Infants Aged 0 to 6 Years
ClinicalTrials.gov study NCT05040542. IPD Sharing: NO. Countries: 1. Publications: 10.
BrainAgeMS - a Comparative Study of Brain Aging in Healthy and Patients With Multiple Sclerosis
ClinicalTrials.gov study NCT06221631. IPD Sharing: YES. Countries: 1. Publications: 3.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.