Decoding Alzheimer's genetic risk through intercellular communication in the human brain: Lessons from Clusterin.

Abstract excerpt

Late-onset Alzheimer's disease (AD) arises in part from a complex genetic architecture dominated by common, low-penetrance variants, many of which are enriched in glial cells and remain mechanistically unresolved. Unlike the rare coding mutations that contribute to early-onset AD, these common variants often lie in noncoding regions, complicating efforts to link genetic risk to cellular function. Emerging...

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