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ScRNAseq of Cd45+ cells from brains of Aducanumab-treated ApoE-variant Alzheimer's mice

ABSTRACT: Here we perform single cell sequencing to examine the impact of aducanumab treatment on the transcriptome of immune cells of aged AD mice bearing knock-in of human APOE variants in the murine APOE locus, treated either with aducanumab or an IgG control.

ORGANISM(S): Mus musculus

PROVIDER: GSE239975 | GEO | 2023/12/29

REPOSITORIES: GEO

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scRNAseq of Cd45+ cells from brains of ApoE-variant Alzheimer's mice sorted by ex-vivo amyloid beta uptake

Project description:Here we perform single cell sequencing of immune cells of aged AD mice bearing knock-in of human APOE variants in the murine APOE locus, sorted into high-uptake and low-uptake pools after incubation with fluorescently labeled amyloid beta.

2023-12-29 | GSE239974 | GEO

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Project description:Here we analyze the gene expression and chromatin accessibility landscape of immune cells in the brains of 5XFAD mice, a common model of Alzheimer's disease, bearing knock-in of human APOE variants in the mouse APOE locus, and aged to 10, 20, 60, or 96 weeks of age.

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scRNAseq of Cd45+ cells from brains of Aducanumab-treated ApoE-variant Alzheimer's mice

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Project description:The most common genetic risk factor for late onset Alzheimer Disease (AD) is the APOE4 allele, with evidence for gain- and loss-of-function as a primary mechanism. ApoE knockout in mice abrogates AD phenotypes but causes severe atherosclerosis due to the role of liver ApoE in cholesterol homeostasis. Previous attempts to therapeutically block brain-specific ApoE in adult models of AD only modestly reduced ApoE expression and no significant impact on amyloid burden. Here, we optimized a divalent siRNA (di-siRNA) to selectively silence ApoE in brain (>2 months). By measuring transcriptomic changes upon knockdown of ApoE in the CNS in multiple mouse models of AD, we find that ApoE knockdown results in an upregulation of the innate immune response, likely through activation of microglia. Additionally, we find that the changes in the transcriptome were similar, but not identical, two weeks and two months post-treatment. We find that mild reduction of ApoE in the liver does not cause widespread transcriptomic changes, but near complete knockdown of ApoE in the liver results in the dysregulation of many lipid metabolism-related pathways.

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