MALT1 and Alzheimer disease: Our findings provide several important contributions: (i) We provide new insights into the causal role of CSF metabolites in AD pathogenesis; (ii) we identify transcriptomic and immune signatures associated with disease progression and develop a predictive model with potential clinical applicability; (iii) we demonstrate that MALT1 overexpression exacerbates neuroinflammation, neuronal injury, and mitochondrial dysfunction in an AD mouse model, and explore its potential as a therapeutic target through molecular docking analyses.