Epidemiological and mouse model data implicate gut dysbiosis in AD pathogenesis years before symptom onset. However, distinguishing causal metabolites from bystander biomarkers requires mechanistic evidence. Butyrate, TMAO, and serotonin precursors have been flagged but causal dose-response relationships in humans remain unclear.
Emerging evidence suggests gut microbial metabolites (SCFAs, TMAO, tryptophan metabolites) may influence amyloid-beta aggregation and neuroinflammation years before clinical symptoms, but causal mechanisms are poorly defined.