Differential expression contributing to memory impairment in AD context
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA614553 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Amyloid plaques and neurofibrillary tangles are present in the brains of individuals with intact memory function. The study of these brains can open new avenues to identify new therapeutic targets. This experriment aimed to identified genes contributing to maintain an intact memory in the presence of AD pathology.
2020-05-07 | GSE147434 | GEO
Project description:The mechanisms underlying age-associated memory impairment are not well understood. We have shown that the onset of memory disturbances in the aging brain is associated with altered hippocampal chromatin plasticity. During learning, aged mice display a specific deregulation of histone H4 lysine 12 (H4K12) acetylation. To analyze if deregulated H4K12 acetylation impacts on learning-induced gene-expression required for memory consolidation we performed a high-density oligonucleotide microarray to compare the entire hippocampal gene-expression profile of 3 and 16-month-old mice during memory consolidation. In order to identify genes differentially regulated between 3- and 16-month old mice upon fear conditioning we subjected 3- and 16-month old mice to fear conditioning (4 mice each group, total 8 mice) . Mice of the same age that were handled but not subjected to any of the employed behavior paradigms served as control (4 mice 3-month old and 4 mice 16-month old, total 8 mice). During fear conditioning mice are subjected to a novel context followed by a mild electric foot-shock (context-shock exposure). In order to identify genes that are differentially regulated upon fear conditioning and are specific to associative learning we also tested the hippocampal gene-expression profile of 3-month old mice subjected to the same context-exposure that is not followed by a foot-shock (Context-exposure) (4 mice) or receive an immediate foot shock once they are placed in the context and only afterwards are allowed to explore the context (shock-context exposure) (4 mice). In order to identify genes that are regulated upon fear conditioning and are specific to associative learning we compared the hippocampal gene-expression profile of mice subjected to fear conditioning (context-shock), context or shock-context exposure regarding to their age-matched control mice (3 month old) mentioned above (control). Hippocampi from each mice were tested resulting to 24 samples which were separately hybridized (OneColor Array Design).
2010-04-28 | E-GEOD-20270 | biostudies-arrayexpress
Project description:Total RNA sequencing of cultured OM cells derived from patients with Alzheimer's disease (AD), individuals with mild cognitive impairment (MCI) and cognitively healthy controls.
| EGAS00001006195 | EGA
Project description:Alzheimer case-control samples originate from the EU funded AddNeuroMed Cohort, which is a large cross-European AD biomarker study relying on human blood as the source of RNA. The design is case-control. Cases are either Alzheimer's disease patients, subjects with mild cognitive impairment or age and gender matched controls.
2015-08-05 | E-GEOD-63061 | biostudies-arrayexpress
Project description:Predisposition to Alzheimer's disease (AD) may arise from lipid metabolism perturbation, however, the underlying mechanism remains elusive. Here, we identify ATAD3A, a mitochondrial AAA-ATPase, as a molecular switch that links cholesterol metabolism impairment to AD phenotypes. In neuronal models of AD, the 5XFAD mouse model and post-mortem AD brains, ATAD3A is oligomerized and accumulated at the mitochondria-associated ER membranes (MAMs), where it induces cholesterol accumulation. Suppressing ATAD3A oligomerization by heterozygous ATAD3A knockout normalizes brain cholesterol turnover and MAM integrity, suppresses APP processing and synaptic loss, and consequently reduces AD neuropathology and cognitive deficits in AD transgenic mice. These findings reveal a role for ATAD3A oligomerization in AD pathogenesis and suggest ATAD3A as a potential therapeutic target for AD.
2022-02-11 | PXD031523 | Pride
Project description:Genome-wide profiling of DNA methylation in blood leukocytes from Chinese patients with mild cognitive impairment (MCI) and Alzheimer’s disease (AD). The Illumina Infinium MethylationEPIC BeadChip array (850K chip) was used to detect DNA methylation profiles throughout approximately 850,000 CpG sites in peripheral blood white cells of MCI- and AD-affected Chinese patients, as well as cognitively healthy controls. All samples included 20 Chinese patients with MCI, 20 Chinese patients with AD, and 20 cognitively healthy controls.
2023-09-11 | GSE208623 | GEO
Project description:We have generated human olfactory neurosphere-derived (ONS) cells from individuals with AD or mild cognitive impairment (MCI), and their cognitively healthy controls, and performed global RNA sequencing to determine gene expression changes in ONS cells.
| EGAS00001006594 | EGA
Project description:Alzheimer's disease (AD) is a neurodegenerative disorder and the most common cause of dementia worldwide. In AD, neurodegeneration spreads throughout the brain cortex in a gradual and predictable pattern, causing progressive memory decline and cognitive impairment. Here, we conducted proteomic, acetylomic and phosphoproteomic analyses of human postmortem tissue samples from AD (Braak stage III-IV) and control brains, covering all anatomical areas affected during the limbic stage of the disease (total hippocampus, CA1, entorhinal and perirhinal cortices). A total of 58 tissues were analyzed by nanoLC-MS/MS.
2021-12-30 | PXD027173 | Pride
Project description:Very little studies have explored the role played by the specialized choroid plexus epithelial cells and the ependymal cells that line the ventricles. In normal and pathological (AD) ageing, reports of alterations in the blood brain CSF barrier (BCSFB) integrity and membrane transporters, accompanied by deficiencies in CSF production and an enlarged ventricular volume have been documented. The molecular sequelae of events driving these age-related pathological changes remains elusive. Given the pivotal role of the ventricular system in normal brain physiology, in this study we proposed to explore their contributing role towards AD pathogenesis. To address this, we used our state-of-the-art proteomic platform, a liquid chromatography/mass spectrometry (LC-MS) approach coupled with Tandem Mass Tag labeling technology to conduct a detailed characterization and assessment of molecular changes in protein expression levels from isolated tissue from the walls of the ventricles in autopsy AD cases, and two groups of age-matched control cases (non-agenarian’s with no AD pathology, and those with no clinical AD diagnosis but significant amyloid pathology and Braak staging).
2021-09-08 | PXD012059 | Pride
Project description:The impact of alcohol abuse on AD is poorly understood. Here we show that the onset of neurocognitive impairment in a mouse model of AD is hastened by repeated alcohol intoxication through exposure to alcohol vapor and we provide a comprehensive gene expression dataset of the prefrontal cortex by single nucleus RNA sequencing of 113,242 cells. Several genes previously associated with AD in humans by GWAS were differentially regulated in specific neuronal populations. Gene expression patterns of AD mice with a history of alcohol intoxication were more similar to the gene expression signatures of older AD mice with more advanced disease and cognitive impairment than to those of younger AD mice with prodromic disease, suggesting that alcohol promotes transcriptional changes consistent with AD progression. Our gene expression dataset at the single cell level provides a unique resource for investigations of the molecular bases of the detrimental role of excessive alcohol intake in AD.
2023-06-09 | GSE218309 | GEO