Aberrant phase separation from a rare ABI3 mutation drives microglial dysfunction and Alzheimer's risk
Although the ABI3 S209F variant is a recognized genetic risk for Alzheimer's disease (AD), its pathogenic mechanism remains elusive.
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Although the ABI3 S209F variant is a recognized genetic risk for Alzheimer's disease (AD), its pathogenic mechanism remains elusive.
LEVs are identified as a critical vesicle subtype mediating the effects of SIRT2 knockdown and support a cell-free therapeutic strategy for AD centered on EVs-driven metabolic reprogramming of microglia.
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