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What makes this convergence striking: 23andMe used bottom-up population genetics (GWAS, n=27,885) VincoPath used top-down proteome interaction mapping Both independently point to GLP-1R signal strength as the rate-limiting variable Neither alone is sufficient genotype determines receptor density, proteome determines signaling threshold For the Alzheimer's field specifically: EVOKE enrolled 3,808 patients without genetic or proteomic stratification

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How do GLP-1 medicines interact with immune cells to reduce #inflammation