Cortex DNA methylation profiles for the Brains for Dementia research cohort
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE197305 | GEO | 2022/06/27
REPOSITORIES: GEO
Similar Datasets
Project description:Cortex DNA methylation profiles for the Brains for Dementia research cohort
| PRJNA809726 | ENA
Project description:We describe in vivo follow-up PET imaging and postmortem findings from an autosomal dominant Alzheimer’s disease (ADAD) PSEN1 E280A carrier who was also homozygous for the APOE3 Christchurch (APOE3ch) variant and was protected against Alzheimer’s symptoms for almost three decades beyond the expected age of onset. We identified a distinct anatomical pattern of tau pathology with atypical accumulation in vivo and unusual postmortem regional distribution characterized by sparing in the frontal cortex and severe pathology in the occipital cortex. The frontal cortex and the hippocampus, less affected than the occipital cortex by tau pathology, contained Related Orphan Receptor B (RORB) positive neurons, homeostatic astrocytes and higher APOE expression. The occipital cortex, the only cortical region showing cerebral amyloid angiopathy (CAA), exhibited a distinctive chronic inflammatory microglial profile and lower APOE expression. Thus, the Christchurch variant impacts the distribution of tau pathology, modulates age at onset, severity, progression, and clinical presentation of ADAD, suggesting possible therapeutic strategies.
2022-08-26 | GSE206744 | GEO
Project description:Gene expression profiling was performed on frontal and temporal cortex from vascular dementia (VaD), Alzheimer's disease (AD), and non-demented controls (Control) obtained from the University of Michigan Brain Bank. Controls and AD cases had no infarcts in the autopsied hemisphere. Vascular dementia cases had low Braak staging.
2019-04-23 | GSE122063 | GEO
Project description:We investigated transcriptome alterations in the prefrontal cortex (BA) of patients with Alzheimer’s disease (AD), dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) when compared with elderly controls without neurological or psychiatric diseases (CTRL) using Affymetrix Human Transcriptome Array 2.0 All brain samples were provided by the Brains for Dementia Research (BDR), UK. All cases were prospectively assessed by experienced clinicians using validated clinical rating instruments. The samples processed in each group were matched for age, sex and postmortem interval (PMI) as far as possible.
2021-05-24 | GSE150696 | GEO
Project description:Four sets of six microarray experiments were conducted. Six individual RTT frontal cortices were co-hybridized with six individual control frontal cortices. For example, the frontal cortex of patient RTT1 was compared with the occipital cortex of RTT1. Additionally, where the frontal cortex of a RTT sample was compared to the frontal cortex of a control sample, the comparison between the occipital cortices was conducted between the same samples. For example RTT1 frontal cortex vs. Con4 frontal cortex, RTT1 occipital cortex vs. Con4 occipital cortex. Each experiment was repeated and the fluorescent cyanine dyes were reversed.
2010-03-07 | E-MEXP-2588 | biostudies-arrayexpress
Project description:Frontotemporal dementia (FTD) is the second most prevalent form of early-onset dementia, affecting predominantly frontal and temporal cerebral lobes. Heterozygous mutations in the progranulin gene (GRN) cause autosomal-dominant FTD (FTD-GRN), associated with TDP-43 inclusions, neuronal loss, axonal degeneration and gliosis, but FTD-GRN pathogenesis is largely unresolved. Here we report single-nucleus RNA sequencing of microglia, astrocytes and the neurovasculature from frontal, temporal and occipital cortical tissue from control and FTD-GRN brains. We show that fibroblast and mesenchymal cell numbers were enriched in FTD-GRN, and we identified disease-associated subtypes of astrocytes and endothelial cells. Expression of gene modules associated with blood–brain barrier (BBB) dysfunction was significantly enriched in FTD-GRN endothelial cells. The vasculature supportive function and capillary coverage by pericytes was reduced in FTD-GRN tissue, with increased and hypertrophic vascularization and an enrichment of perivascular T cells. Our results indicate a perturbed BBB and suggest that the neurovascular unit is severely affected in FTD-GRN.
2022-06-03 | GSE163122 | GEO
Project description:Around 25% of stroke survivors over 65 years old develop progressive cognitive decline more than 3 months post-stroke, with features of vascular dementia. Poststroke dementia (PSD) is associated with pathology in frontal brain regions, in particular dorsal lateral prefrontal cortex (DLPFC) neurons and white matter, remote from the infarct, implicating damage to anterior cognitive circuits (ACC) involved in impaired executive function. We hypothesised that PSD results from progressive neuronal damage in the DLPFC and that this is associated with alterations in the gliovascular unit (GVU) of frontal white matter. We aimed to identify the cellular and molecular basis of PSD by investigating the transcriptomic profile of the neurons and white matter GVU cells previously implicated in pathology. Laser capture microdissected neurons, astrocytes and endothelial cells were obtained from the Cognitive Function After Stroke (COGFAST) cohort. Gene expression was assessed using microarrays and pathways analysis to compare changes in PSD with controls and with poststroke non-dementia (PSND). Laser captured microdissected neurons were obtained from the bilateral carotid artery stenosis (BCAS) model and equivalent SHAM animals
2022-06-01 | GSE186798 | GEO
Project description:Alzheimer’s disease (AD) and Lewy body dementia (LBD) are two different forms of dementia but their pathology may involve the same cortical areas with overlapping cognitive manifestation. Dementia cases within the same family share a common genetic background. Nonetheless, the clinical phenotype may be different due to the different underlying molecular processes that come-up apart from genetics, causing diverse neurodegeneration. Through neuropathological, genetic and transcriptomic comparison of four different brain areas (substantia nigra, hippocampus, parietal lobe and basal ganglia), we defined commonalities and differences in the pathological processes of dementia in two kindred cases, a mother and a son, who developed a classical AD and an aggressive form of AD/LBD respectively. Genetic analysis did not reveal any pathogenic variants in the principal AD/LBD-causative genes. RNA sequencing highlighted high transcriptional dysregulation within the substantia nigra in LBD pathology, while AD underwent lower degree of transcriptional dysregulation, with the parietal lobe being the most involved brain area. Conversely, hippocampus (the most degenerated area) and basal ganglia (lacking specific lesions) expressed the lowest level of dysregulation. Our data suggest that there is a link between the transcriptional dysregulation and the amount of tissue damage accumulated across time, assessed through neuropathology. Moreover, we highlight that the molecular bases of AD and LBD follow very different pathways, which underlie their neuropathological signatures. Indeed, the transcriptome profiling through RNA sequencing may be an important tool in flanking the neuropathological analysis for a deeper understanding of AD and LBD pathogenesis.
2022-08-03 | GSE193438 | GEO
Project description:The Aging, Dementia and Traumatic Brain Injury Study is a detailed neuropathologic, molecular and transcriptomic characterization of brains of control and TBI exposure cases from a unique aged population-based cohort from the Adult Changes in Thought (ACT) study. This study was developed by a consortium consisting of the University of Washington, Kaiser Permanente Washington Health Research Institute, and the Allen Institute for Brain Science, and was supported by the Paul G. Allen Family Foundation. This freely available resource (http://aging.brain-map.org/) presents a systematic and extensive data set of study participant metadata, quantitative histology and protein measurements of neuropathology, and RNA sequencing (RNA-seq) analysis of hippocampus and neocortex. Specific methodological details are available on the “Documentation” tab at http://aging.brain-map.org/. Included in this data set are normalized RNA-Seq FPKM files used for analysis in "Neuropathological and transcriptomic characteristics of the aged brain", published in eLife. Other processed data files as well as sample and donor meta-data and QC metrics are available at http://aging.brain-map.org/download/index Controlled access to raw data files is available via https://www.niagads.org/datasets/ng00059
2017-10-16 | GSE104687 | GEO
Project description:Aging, Dementia, and TBI Study
| PRJNA413517 | ENA