Mechanistically, we observed that UA treatment mitigated oligomeric Aβ‐induced downregulation of phagocytic receptors, including CD36, MSR1, and ABCA7, aligning with previous observations in AD mice.[31] In vitro phagocytosis assays revealed that UA enhances Aβ phagocytosis by restoring impaired recycling of CD36 and TREM2. The gene discussed is TREM2; the disease is Alzheimer disease.