TFEB and Parkinson disease: A recent study has demonstrated that UA serves as a TFEB activator, thereby promoting microglial autophagy and enhancing Aβ clearance.[65] Furthermore, UA has been reported to suppress microglial inflammatory cytokine production and protect dopaminergic neurons in Parkinson's disease.[39] Given that UA accounts for 60% of total plasma antioxidant capacity, it may protect the brain from Aβ toxicity and glial neuroinflammation; however, this hypothesis warrants further investigation.