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Expression data from Alzheimer's disease model mouse

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE36981 | GEO | 2013/04/17

SECONDARY ACCESSION(S): PRJNA157437

REPOSITORIES: GEO

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Expression data from Alzheimer's disease model mouse

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 AlzheimerM-bM-^@M-^Ys disease. 3xTg-AD-H mice harboring a homozygous Psen1M146V mutation and homozygous mutant transgenes for APPSwe and tauP301L, 3xTg-AD-h mice harboring hemizygous APPSwe and tauP301L transgenes with a homozygous Psen1M146V mutation, and non-transgenic control mice (non-Tg) were used in this study, (male, n=3 for each group). RNA samples prepared from hippocampi were subjected to microarray analysis using the Affymetrix Mouse Gene 1.0 ST platform (GPL6246).

2013-04-17 | E-GEOD-36981 | biostudies-arrayexpress

Expression data from post mortem Alzheimer's disease brains

2013-04-17 | GSE36980 | GEO

Expression data from post mortem Alzheimer's disease brains

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

MTH1 and OGG1 maintain a low level of 8-oxoguanine in Alzheimer's brain, and prevent the progression of Alzheimer's pathogenesis

Project description:To investigate the role of 8-oxo-7, 8-dihydroguanine (8-oxoguanine) accumulation in DNA or nucleotide pools during the development of AD pathology, we introduced a Mth1/Ogg1-double deficiency into homozygous triple-transgenic AD model (3xTg-AD-H) mice. Mth1 encodes 8-oxo-7, 8-dihydro-2'-deoxyguanosine-5'-triphosphatase (8-oxo-dGTPase) and Ogg1 encodes 8-oxoguanine DNA glycosylase 1. One-way eBays ANOVA of microarray data from hippocampi revealed that the gene expression profiles are most significantly altered in the hippocampi of 3xTg-AD-H with Mth1/Ogg1-double deficient (ADH/TO-DKH) mice compared to non-Tg control (NT) mice. Comparative analysis between 3xTg-AD-H (ADH/WT) and ADH/TO-DKH mice showed that the expression of genes involved in neuroprotection are significantly altered. Among them, expression of the AD-related genes including Ttr, Enpp2, Kcnj13 and Kl was significantly downregulated in ADH/TO-DKH mice.

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Comparative profiling of hippocampal gene expression in AppNL-G-F knock-in mouse model of Alzheimer's disease.

Project description:To identify molecular pathological alterations in Alzheimer’s disease (AD) brains, we had previously performed comparative gene expression profiling with human gene array using RNAs prepared from postmortem human brains donated for the Hisayama study. The hippocampi from AD brains showed the most significant alteration in gene expression profile (PMID: 23595620). In the present study, in order to obtain a comprehensive view of gene expression profiles in AD hippocampus, we applied human transcriptome array and deep RNA-sequencing to the same samples and reanalyzed the gene array data, and performed integrative analysis of all 3 methods. We also applied gene array to hippocampus of 6-month-old App[NL-G-F/NL-G-F] knock-in AD model mice, and at last we performed the interspecies comparison. IPA analysis of the top significantly altered genes derived from integrative analysis of all 3 methods in human AD hippocampus revealed that neurotransmission, synaptic transmission and development of neurons are the top significantly decreased functions. In hippocampi of App[NL-G-F/NL-G-F] mice which exhibit significant amyloidosis but not neuronal degeneration, we found that expression of Gfap (astrocyte marker) and Cd68 (microglia marker) genes are significantly upregulated together with genes categorized in the immune response of cells. Comparing the human and mouse data, we found major common genes are related to recruitment of inflammatory cells. Amyloid-beta accumulation is the major hallmark of AD at 6 month-old App[NL-G-F/NL-G-F] mice, therefore our data suggests that amyloid-beta accumulation increases the recruitment of inflammatory cells in early stage of AD brain, prior to neuronal degeneration.

2021-12-01 | GSE157161 | GEO

Comparative profiling of cortical gene expression in Alzheimer's disease patients and mouse models demonstrates a link between amyloidosis and neuroinflammation

Project description:Alzheimer's disease (AD) is the most common form of dementia, characterized by accumulation of amyloid beta (Abeta) and neurofibrillary tangles. Oxidative stress and inflammation are considered to play an important role in the development and progression of AD. However, the extent to which these events contribute to the Abeta pathologies remains unclear. We performed inter-species comparative gene expression profiling between AD patient brains and the App (NL-G-F/NL-G-F) and 3xTg-AD-H mouse models. Genes commonly altered in App (NL-G-F/NL-G-F) and human AD cortices correlated with the inflammatory response or immunological disease. Among them, expression of AD-related genes (C4a/C4b, Cd74, Ctss, Gfap, Nfe2l2, Phyhd1, S100b, Tf, Tgfbr2, and Vim) was increased in the App (NL-G-F/NL-G-F) cortex as Abeta amyloidosis progressed with exacerbated gliosis, while genes commonly altered in the 3xTg-AD-H and human AD cortices correlated with neurological disease. The App (NL-G-F/NL-G-F) cortex also had altered expression of genes (Abi3, Apoe, Bin2, Cd33, Ctsc, Dock2, Fcer1g, Frmd6, Hck, Inpp5D, Ly86, Plcg2, Trem2, Tyrobp) defined as risk factors for AD by genome-wide association study or identified as genetic nodes in late-onset AD. These results suggest a strong correlation between cortical Abeta amyloidosis and the neuroinflammatory response and provide a better understanding of the involvement of gender effects in the development of AD.

2017-12-21 | GSE92926 | GEO

Application of short-RNA-seq in post-mortem human hippocampi from the Calgary Brain Bank (CBB) to assess transcriptome-wide deregulation in processing of SINE Alu RNAs in AlzheimerÃ¢Â€Â™s disease

Project description:Here, we investigate through short-RNA_seq in human hippocampi from the Calgary Brain Bank (CBB) whether Alu RNAs are processed in human brains, and whether their processing ratio is deregulated in brains of AD patients compared to healthy aging individuals.

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Expression data from Alzheimer's disease (AD) model mouse and AD model mouse overexpressing human mitochondrial transcriptional factor A (hTFAM)

Project description:To delineate the mechanism underlying the amelioration of AD pathophysiology by hTFAM, we performed gene expression profiling using hippocampal RNAs from the AD model mouse and AD model mouse overexpressing human TFAM. One-way ANOVA of microarray data from hippocampus revealed that the gene expression profile is most significantly altered in the hippocampi of ADh/hTFAMh mice. Comparative analyses of the brains of ADh/WT and ADh/hTFAMh mice showed that the expression of genes involved in cancer, endocrine system disorders, and organismal injury and abnormalities were significantly altered. Among the genes whose expression was significantly altered by hTFAM expression, transthyretin, encoded by the Ttr gene, binds Aβ and inhibits its aggregation.

2016-12-01 | GSE80242 | GEO

Integrative analysis of altered genes expressed in human Alzheimer’s disease brain (RNA-Seq)

Project description:We had previously performed comparative gene expression profiling of human postmortem Alzheimer’s disease (AD) brains donated for the Hisayama study. The hippocampi from AD brains showed the most significant alteration in gene expression profile [PMID: 23595620]. In the present study, in order to identify molecular pathological alterations in AD hippocampus, we applied human transcriptome array and RNA-sequencing to the same samples and reanalyzed the gene array data, and performed integrative analysis of all 3 methods. We also applied gene array to hippocampus of 6-month-old AppNL-G-F/NL-G-F knock-in AD model mice as a preclinical AD stage model, and at last we performed the interspecies comparison. Functional annotation clustering with the results of all 3 or at least 2 methods in human, showed synapse, cell junction, calmodulin binding, ion transport and glycoproteins as the top affected terms. In hippocampi of AppNL-G-F/NL-G-F mice which exhibit significant amyloidosis but not neuronal degeneration, we found that expression of genes categorized in signaling specially signaling peptides with disulfide bond or glycoproteins, together with the innate immune response and lysosome of cells are upregulated. Comparing the extended human data with mouse data, we found and confirmed by qRT-PCR, 2 common up-regulated genes, Clec7a and C4b, which induce innate immune response and synapse elimination. We also found and confirmed by qRT-PCR, 2 common down-regulated genes, one is Slc17a6, which can affect synaptic transmission of glutamate, and second one is Rxfp1, which is involved in gene transcription. Amyloid- accumulation is the major hallmark of AD at 6 month-old AppNL-G-F/NL-G-F mice, therefore our data suggests that amyloid- accumulation induces innate immune response, synapse elimination, besides it can decreases glutamate transmission, and affect gene transcription in early stage of hippocampal AD brain, prior to neuronal degeneration.

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Whole hippocampus RNA seq on (SCDi Cayman 10566) and Vehicle (DMSO) in 10 month old WT and 3xTg-AD mice

Project description:RNA was extracted from microdissected hippocampi from 10-month old DMSO or SCDi (Cayman 10566) ICV treated WT or 3xTg-AD mice.

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