Based on current evidence, we propose several potential mechanisms that warrant further validation: 1) impaired purine metabolism through reduced xanthine oxidase activity or upstream disturbances,[57] 2) accelerated oxidative degradation, given UA's role as a major endogenous antioxidant in the high‐oxidative‐stress AD environment, 3) enhanced renal/cerebral excretion via overexpressed ABCG2 and MRP4 transporters reported in AD brain,[58, 59] and 4) APOE4 genotype association with lower SUA levels compared to APOE2 carriers.[60]. This evidence concerns the gene ABCG2 and Alzheimer disease.