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Molecular neurobiology · Apr 2017
Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5×FAD Transgenic Mice.
- Kunmu Zheng, Xiaoman Dai, Nai'an Xiao, Xilin Wu, Zhen Wei, Wenting Fang, Yuangui Zhu, Jing Zhang, and Xiaochun Chen.
- Department of Neurology and Geriatrics, Fujian Institute of Geriatrics, Affiliated Union Hospital of Fujian Medical University, 29 Xinquan Road, Fuzhou, Fujian, 350001, People's Republic of China.
- Mol. Neurobiol. 2017 Apr 1; 54 (3): 1967-1977.
AbstractAlzheimer'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 β-amyloid protein (Aβ) 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 5×FAD 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 Aβ production by downregulating BACE1 expression, preventing synaptic degradation, and improving spatial learning and memory impairment of 5×FAD mice. These findings suggest that curcumin is a potential candidate for AD treatment.
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