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- W3157602736 abstract "Selective neurodegeneration is a critical causal factor in Alzheimer's disease (AD); however, the mechanisms that lead some neurons to perish, whereas others remain resilient, are unknown. We sought potential drivers of this selective vulnerability using single-nucleus RNA sequencing and discovered that ApoE expression level is a substantial driver of neuronal variability. Strikingly, neuronal expression of ApoE-which has a robust genetic linkage to AD-correlated strongly, on a cell-by-cell basis, with immune response pathways in neurons in the brains of wild-type mice, human ApoE knock-in mice and humans with or without AD. Elimination or over-expression of neuronal ApoE revealed a causal relationship among ApoE expression, neuronal MHC-I expression, tau pathology and neurodegeneration. Functional reduction of MHC-I ameliorated tau pathology in ApoE4-expressing primary neurons and in mouse hippocampi expressing pathological tau. These findings suggest a mechanism linking neuronal ApoE expression to MHC-I expression and, subsequently, to tau pathology and selective neurodegeneration." @default.
- W3157602736 created "2021-05-10" @default.
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- W3157602736 date "2021-05-06" @default.
- W3157602736 modified "2023-10-14" @default.
- W3157602736 title "Neuronal ApoE upregulates MHC-I expression to drive selective neurodegeneration in Alzheimer’s disease" @default.
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- W3157602736 doi "https://doi.org/10.1038/s41593-021-00851-3" @default.
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