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Supporting this epidemiologic signal, large cohort data also suggest an inverse relationship between GLP-1 exposure and a core pathological hallmark of Alzheimers disease: the accumulation of amyloid in the brain [32].While observational data cannot establish causality, the convergence of reduced clinical incidence and favorable biomarker associations strengthens the case that GLP-1 signaling may be influencing disease-relevant biology rather than serving as a passive metabolic proxy