// Yi-Heng Tai 1, * , Yu-Yi Lin 1, * , Kai-Chen Wang 2, * , Chao-Lin Chang 3 , Ru-Yin Chen 3 , Chia-Chu Wu 3 and Irene H. Cheng 1, 4 1 Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan 2 Department of Neurology, Cheng-Hsin General Hospital, Taipei, Taiwan 3 Food Industry Research and Development Institute, Hsinchu, Taiwan 4 Brain Research Center, National Yang-Ming University, Taipei, Taiwan * These authors have contributed equally to this work Correspondence to: Irene H. Cheng, email: hjcheng@ym.edu.tw Keywords: Alzheimer’s disease; curcuminoid submicron particle; APP transgenic mouse; amyloid; curcumin Received: August 29, 2017 Accepted: January 25, 2018 Published: January 31, 2018 ABSTRACT Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and is triggered via abnormal accumulation of amyloid-β peptide (Aβ). Aggregated Aβ is responsible for disrupting calcium homeostasis, inducing neuroinflammation, and promoting neurodegeneration. In this study, we generated curcuminoid submicron particle (CSP), which reduce the average size to ~60 nm in diameter. CSP had elevated the bioavailability in vivo and better neuroprotective effect against oligomeric Aβ than un-nanosized curcuminoids in vitro . Two months of CSP consumption reversed spatial memory deficits and the loss of a calcium binding protein calbindin-D 28k in the hippocampus of AD mouse model. In addition, CSP consumption lowered amyloid plaques and astrogliosis in vivo and enhanced microglial Aβ phagocytosis in vitro , implying that the beneficial effects of CSP also mediated via modulating neuroinflammation and enhancing amyloid clearance. Taken together, our study demonstrated the protective effects of CSP toward ameliorating the memory impairment and pathological deficits in AD mouse model.
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