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Protection and reversal of excitotoxic neuronal damage by glucagon-like peptide-1 and exendin-4

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Population-scale studies of incretin response, glucagon receptor sensitivity, central appetite-control variants, lipid handling pathways, energy-expenditure-related loci, muscle-preservation genetics, and the cardiovascular-protection signaling that may explain real-world MACE differences, these literatures exist, they are growing, and they are starting to converge on a set of variants whose effect sizes are large enough to influence the prior distribution from which a clinician chooses a starting molecule