Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5xFAD Transgenic Mice

Alzheimer's disease (AD) is the most common dementia and the trigger of its pathological cascade is widely believed to be the overproduction and accumulation of beta-amyloid protein (A beta) in the affected brain. However, effective AD remedies are still anxiously awaited. Recent evidence suggests that curcumin may be a potential agent for AD treatment. In this study, we used 5xFAD transgenic mice as an AD model to investigate the effects of curcumin on AD. Our results showed that curcumin administration (150 or 300 mg/kg/day, intragastrically, for 60 days) dramatically reduced A beta production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5xFAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.