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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.

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Differential and synergistic transcriptional effects of early amyloid-β and tau pathologies in the hippocampus of APP, Tau, and APP/Tau female mice

Project description:Alzheimer’s disease (AD) is characterized by memory loss associated with accumulation of amyloid-β (Aβ) and tau in the brain, but how memory-processing neural circuits are differentially affected by each pathology remains unclear. Here, we investigated the transcriptional vulnerability to single and concomitant Aβ and tau pathologies in 6-month-old transgenic mice expressing mutant human amyloid precursor protein (APP), Tau, or both (APP/Tau mice) in excitatory neurons. We identified differential and synergistic pathology-induced transcriptional responses in the hippocampus of AD transgenic mice. These findings support the idea that Aβ and tau pathologies exert synergistic effects to disrupt gene expression programs underlying vulnerability of memory neural circuits in AD.

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Transcriptional vulnerability to amyloid-β and tau pathologies differentially disrupts emotional and memory neural circuits

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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.

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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).

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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.

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Mus musculus

Project description:Expression profile of microglia from Egln3–/–, App-Psen1 and App-Psen1

| PRJNA381764 | ENA