Abstract
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 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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Acknowledgments
We thank Prof. Mary Jo LaDu (Department of Anatomy and Cell Biology, University of Illinois at Chicago, USA) for kindly providing the 5×FAD mice. These studies were funded by the National Natural Science Foundation of China to Prof. Xiao-chun Chen (No. 91232709, 811171216, 81110555) and Prof. Jing Zhang (No. 81401149) and the National and Fujian Province’s Key Clinical Specialty Discipline Construction Programs.
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Kunmu Zheng and Xiaoman Dai contributed equally to this work.
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Zheng, K., Dai, X., Xiao, N. et al. Curcumin Ameliorates Memory Decline via Inhibiting BACE1 Expression and β-Amyloid Pathology in 5×FAD Transgenic Mice. Mol Neurobiol 54, 1967–1977 (2017). https://doi.org/10.1007/s12035-016-9802-9
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DOI: https://doi.org/10.1007/s12035-016-9802-9