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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A Genome-wide Gene Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

ABSTRACT: The purpose of this project was to compare whole genome expression in 5 transgenic mice with human genes for dementia that result in either plaques or tangle pathology to the expression in wild-type control mice and to each other at different stages of disease progression. Total RNA was obtained from hippocampus, cortex and cerebellum in four lines of ‘amyloid’ transgenic mice (mutant human APP and APP/PSEN1 genes) and ‘TAU’ transgenic mice (mutant human MAPT gene) as well as wild-type control mice at 8,16, 32 and 72 weeks

ORGANISM(S): Mus musculus

SUBMITTER: Frances Edwards

PROVIDER: E-GEOD-64398 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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A Genome-wide Gene Expression Analysis and Database in Transgenic Mice during Development of Amyloid or Tau Pathology

Project description:The purpose of this project was to compare whole genome expression in 5 transgenic mice with human genes for dementia that result in either plaques or tangle pathology to the expression in wild-type control mice and to each other at different stages of disease progression.

2014-12-24 | GSE64398 | GEO

APP levels mediate beta-amyloid but not tau-related aspects of Alzheimer’s disease in a Down syndrome model of cortical neurogenesis.

Project description:Early-onset Alzheimer’s disease-like pathology in Down syndrome (DS, trisomy 21) is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene. To test this central tenet of the amyloid-cascade hypothesis we deleted the supernumerary copy of the APP gene in trisomic DS iPSC, or upregulated APP expression in euploid human pluripotent stem cell lines with dCas9-VP64, and subjected these lines to prolonged cortical neural differentiation. Our data reveal that increased APP gene dosage and expression is necessary and sufficient for increased beta-amyloid production and pyroglutamate(E3)-containing plaque deposition, but is neither sufficient nor required for tau hyperphosphorylation, neurofibrillary tangle formation, or increased oxidative stress-induced apoptosis in neurons. Transcriptome comparisons of the isogenic neurons demonstrates that the supernumerary APP gene copy has profound temporally-modulated genome-wide effects on gene expression during differentiation and maturation of DS neuronal cultures that link APP function to regulation of genes involved in neuronal synaptic function and outgrowth of neuronal processes. Collectively, our data reveal that APP plays an important role in the amyloidogenic aspects of Alzheimer’s disease, but challenge the hypothesis that increased APP levels are solely responsible for hyperphosphorylation of tau or enhanced oxidative stress-induced neuronal cell death in Down syndrome associated AD-pathogenesis.

2018-06-12 | GSE100680 | GEO

Genome-wide H3K27ac profiles in post-mortem entorhinal cortex samples from Alzheimer's disease cases and controls

Project description:We quantified genome-wide levels of H3K27ac in post-mortem entorhinal cortex tissue samples, identifying widespread Alzheimer's disease (AD)-associated acetylomic variation. Differentially acetylated peaks were identified in the vicinity genes implicated in both tau and amyloid neuropathology (MAPT, APP, PSEN1, PSEN2), as well as genomic regions containing variants associated with sporadic late-onset AD (CR1, TOMM40). Both MAPT and PSEN2 are characterized by an extended hyperacetylated region upstream of the TSS mapping to enhancers in the brain. We show that genes annotated to AD-associated hyper- and hypoacetylated peaks are enriched for brain- and neuropathology-related functions.

2018-08-11 | GSE102538 | GEO

Study on brain phosphorylation proteomics of transgenic mice with early Alzheimer's disease

Project description:Alzheimer’s disease (AD) is the most common neurodegenerative disorder caused by multiple pathological factors such as the overproduction of β-amyloid (Aβ) and the hyperphosphorylation of tau. However, there is limited knowledge of the mechanisms underlying AD pathogenesis and no effective biomarker for the early diagnosis of this disorder. In this study, we performed a quantitative phosphoproteomic analysis for the evaluation of global protein phosphorylation in the hippocampus of Aβ overexpression APP/PS1 transgenic mice, and tau overexpression MAPT×P301S transgenic mice, respectively. These AD mice at ten-week-old did not exhibit cognitive dysfunction and were widely used to simulate AD patients at the early stage. The number of differentially phosphorylated proteins (DPPs) was greater in APP/PS1 transgenic mice than those of MAPT×P301S transgenic mice. And the function of DPPs in APP/PS1 transgenic mice was mainly related to synapse, while the function of DPPs in MAPT×P301S transgenic mice was mainly related to microtubule. In addition, an AD core network containing 7 phosphoproteins differentially expressed in both animal models was established, and the function of this core network related to synapse and oxidative stress. All these results indicated that Aβ and tau might induce different protein phosphorylation profiles in the early stage of AD, leading to the dysfunctions in synapses and microtubule, respectively. And the detection of same DPPs in these animal models might be used for early AD diagnosis.

2023-02-19 | PXD040254 | iProX

Genetic variability in response to Amyloid beta deposition influences Alzheimer's disease risk

Project description:The purpose of this project was to compare whole genome expression in 5 transgenic mice that show either amyloid plaques or tangle pathology to the expression in wild-type control mice at different stages of disease progression (2, 4, 8 or 18 months of age). Mouse genes with expression correlating to pathology were then compared to human genes showing DNA variation in human population associated with dementia (from GWAS).

2019-10-31 | GSE137313 | GEO

DNA methylation profiles across different brain regions in APP/PSEN1 mice

Project description:Genome wide DNA methylation profiling of normal and APP/PSEN1 mice. A custom Illumina Golden Gate DNA methylation Beadchip was used to obtain DNA methylation profiles across approximately 800 CpGs. Bisulphite converted DNA from the 96 samples were hybridised to the Illumina custom golden gate DNA methylation array.

2015-12-05 | E-GEOD-42745 | biostudies-arrayexpress

DNA methylation profiles across different brain regions in APP/PSEN1 mice

2015-12-05 | GSE42745 | GEO

APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [fibroblasts]

Project description:Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most frequent cause of dementia. The disease has a substantial genetic component comprising both highly penetrant familial mutations (APP, PSEN1 and PSEN2) and sporadic cases with complex genetic etiology. Mutations in APP and PSEN1/2 alter the proteolytic processing of APP to its metabolites, including Ab and APP Intracellular Domain (AICD). In this study, we use transgenic porcine models carrying the human APPsw and PSEN1M146I transgenes to demonstrate the pathobiological relevance of transcriptional regulation facilitated by APP and its AICD domain. Through molecular characterization of hippocampal tissue, we describe the differential expression of gene sets that cluster in molecular pathways with translational relevance to AD. We further identify phosphorylated and unphosphorylated AICD in differential complexes with proteins implicated in signal transduction and transcriptional regulation. Integrative genomic analysis of transcriptional changes in somatic cell cultures derived from pigs treated with g-secretase inhibitor demonstrates the importance of g-secretase APP processing in transcriptional regulation. Collectively, our data supports a model in which APP, and in particular its AICD domain, modulates gene networks associated with AD pathobiology through interaction with signaling proteins.

2024-02-04 | GSE254570 | GEO

APP and its intracellular domain modulate Alzheimer’s disease risk gene networks in transgenic APPsw and PSEN1M146I porcine models [hippocampus]

2024-02-04 | GSE254548 | GEO

Untargeted mass spectrometry reveals impact of high fat diet on peripheral amino acid regulation in a mouse model of Alzheimer’s Disease

Project description:APPSwe/PS1ΔE9 (APP/PSEN1) transgenic mice (to represent familial or early-onset AD) and wild-type litter mater controls were fed either a high-fat diet (HFD, 60% kcal from lard), low-fat diet (LFD, 10% kcal from lard) from 2 months of age, or reversal diet (REV, high-fat followed by low-fat from 9.5 months).

2021-06-03 | ST001848 | MetabolomicsWorkbench

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