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This narrative review uniquely addresses how gut microbiota\u2010derived metabolites mediate overlapping pathologies of insulin resistance, neuroinflammation, and amyloidogenesis in T2DM and AD, proposing a framework for dual therapeutic targeting. This narrative review provides an in\u2010depth examination of the roles and mechanisms of gut microbiota and their metabolites in the context of T2DM and AD. This study indicates that gut microbiota dysbiosis significantly impacts the pathogenesis and progression of both diseases by modulating metabolic pathways, immune functions, and inflammatory responses. Key bacteria, such as <jats:italic>Akkermansia muciniphila<\/jats:italic> (which releases outer membrane vesicles), <jats:italic>Lactobacillus<\/jats:italic>, and <jats:italic>Bifidobacterium<\/jats:italic>, as well as their metabolites like short\u2010chain fatty acids (SCFAs), bile acids (BAs), lipopolysaccharide (LPS), vitamins, and Trimethylamine N\u2010oxide (TMAO) regulate T2DM and AD through complex mechanisms. Multiple signaling pathways, including G\u2010protein coupled receptor 41\/43 (GPR41\/43), phosphoinositide 3\u2010kinase (PI3K)\/protein kinase B (Akt), Toll\u2010like receptor 4 (TLR4)\/nuclear factor kappa\u2010light\u2010chain\u2010enhancer of activated B cells (NF\u2010\u03baB), and endoplasmic reticulum (ER) stress\u2010mediated pathways, are also involved. 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