Genome-wide profiling of altered gene expression in the neocortex of Alzheimer's disease (gene level)
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE37263 | GEO | 2012/04/13
SECONDARY ACCESSION(S): PRJNA159153
REPOSITORIES: GEO
Similar Datasets
Project description:We investigated genome-wide gene alterations in the temporal cortex of a well-characterized cohort of Alzheimer’s disease (AD) patients using Affymetrix exon arrays.
2014-06-30 | GSE37264 | GEO
Project description:We investigated genome-wide gene alterations in the temporal cortex of a well-characterized cohort of AlzheimerM-bM-^@M-^Ys disease (AD) patients using Affymetrix exon arrays. The AD patients and controls are subjects originally recruited into OPTIMA (Oxford Project to Investigate Memory and Ageing). Subjects underwent annual clinical and neuropsychological assessments, including the Cambridge Cognitive Examination (CAMCOG). Among subjects who died with autopsy consent given by next of kin, 1 cm3 blocks of grey matter from BA22 were dissected from fresh frozen brains of AD subjects. Tissues from elderly controls, followed longitudinally in life and with CAMCOG scores >80 at the last assessment before death, were collected. Affymetrix exon array was carried out in 8 control and 8 AD samples. The samples processed in each hybridization run were matched for AD vs. control, sex and postmortem interval (PMI) as far as possible. This submission includes the exon-level analysis.
2014-06-30 | E-GEOD-37264 | biostudies-arrayexpress
Project description:We investigated genome-wide gene alterations in the temporal cortex of a well-characterized cohort of AlzheimerM-bM-^@M-^Ys disease (AD) patients using Affymetrix exon arrays. The AD patients and controls are subjects originally recruited into OPTIMA (Oxford Project to Investigate Memory and Ageing). Subjects underwent annual clinical and neuropsychological assessments, including the Cambridge Cognitive Examination (CAMCOG). Among subjects who died with autopsy consent given by next of kin, 1 cm3 blocks of grey matter from BA22 were dissected from fresh frozen brains of AD subjects. Tissues from elderly controls, followed longitudinally in life and with CAMCOG scores >80 at the last assessment before death, were collected. Affymetrix exon array was carried out in 8 control and 8 AD samples. The samples processed in each hybridization run were matched for AD vs. control, sex and postmortem interval (PMI) as far as possible. This submission includes the gene-level analysis.
2012-04-12 | E-GEOD-37263 | biostudies-arrayexpress
Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease. We prepared RNA samples from the gray matter of frontal and temporal cortices and hippocampi derived from 88 postmortem brains, among which 26 cases were pathologically diagnosed as having AD or an AD-like disorder. High-quality RNA (RIN≧6.9) samples were subjected to microarray analysis using the Affymetrix Human Gene 1.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 1.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 33 frontal cortex samples, among which 15 were from AD patients; 29 temporal cortex samples, among which 10 were from AD patients; 17 hippocampus samples, among which seven were from AD patients
2013-04-17 | E-GEOD-36980 | biostudies-arrayexpress
Project description:AD is the leading cause of dementia in the elderly. However, disease etiology is still practically unknown. To gain insight into the molecular mechanisms underlying this disease we used the Affymetrix exon arrays to profile the alternative splicing landscape of human entorhinal cortex samples from AD patients and controls. We found a few hundred events of alternative spicing that characterize the AD entorhinal cortex and may have profound effect on the pathogenesis of this disease. Expression was analyzed using Affymetrix Human Exon 1 S.T arrays samples from 3 female NDCs and 3 female AD patients were included in this study
2012-09-06 | E-GEOD-26972 | biostudies-arrayexpress
Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease.
2013-04-17 | GSE36981 | GEO
Project description:AD is the leading cause of dementia in the elderly. However, disease etiology is still practically unknown. To gain insight into the molecular mechanisms underlying this disease we used the Affymetrix exon arrays to profile the alternative splicing landscape of human entorhinal cortex samples from AD patients and controls. We found a few hundred events of alternative spicing that characterize the AD entorhinal cortex and may have profound effect on the pathogenesis of this disease. Expression was analyzed using Affymetrix Human Exon 1 S.T arrays
2012-09-06 | GSE26972 | GEO
Project description:To identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD) Three-way ANOVA of microarray data from frontal cortex, temporal cortex and hippocampus with presence/absence of AD and vascular dementia, and sex, as factors revealed that the gene expression profile is most significantly altered in the hippocampi of AD brains. Comparative analyses of the brains of AD patients and a mouse model of AD showed that genes involved in non-insulin dependent DM and obesity were significantly altered in both, as were genes related to psychiatric disorders and Alzheimer’s disease.
2013-04-17 | GSE36980 | GEO
Project description:Alzheimer’s disease (AD) is the most common neurodegenerative disorder being characterized by progressive impairment of memory and cognition, resulting in dementia. To investigate brain region vulnerability to AD and which pathways are altered in certain areas in AD, we performed proteomic profiling of human brain samples during AD progression in regions early (medial temporal lobe - MTL) and late affected (neocortex) by tau pathology. We employed a mass spectrometry-based approach to interrogate the human brain proteome during AD progression (B/B stages) in four distinct brain regions: entorhinal cortex (EC), parahippocampal cortex (PHC), temporal cortex (TC) and frontal cortex (FC). Importantly, we wanted to evaluate brain areas that are affected by tau pathology in different disease stages, in order to gain insights if there are common mechanisms or patterns shared between different brain regions during disease progression. A total of 103 samples were analyzed by nanoLC-MS/MS.
2019-07-01 | PXD010138 | Pride
Project description:Amyloid-beta peptides which aggregate and accumulate in Alzheimer’s disease (AD) brain are known to have sequential N-terminal truncations and multiple post-translational modifications (PTM) such as isomerization, pyroglutamate formation, phosphorylation, nitration and dityrosine cross-linking. Here we add to the list of PTM citrullination (deimination) of Arg5 residue in plaque-derived Abeta in sporadic AD brains, identified by tandem mass spectrometry. We quantitated the level of citrullination on multiple N-truncated Abeta isoforms present in plaque-associated fractions and found that almost 30 % of pyroGlu3-Abeta pool was citrullinated in plaques from AD temporal cortex. We also documented citrullinated Abeta peptides in the detergent insoluble fractions from AD frontal cortex with ~ 22 % citrullination in the pyroGlu3-Abeta pool. Citrullination of Abeta is a common PTM, closely associated with pyroglutamate-Abeta formation and Abeta accumulation in AD. This may have implications for Abeta toxicity, auto-antigenicity of Abeta, and may be relevant for the design of diagnostic assays and therapeutic targeting.
2021-11-24 | PXD025620 | Pride