Curcuminoid submicron particle ameliorates cognitive deficits and decreases amyloid pathology in Alzheimer's disease mouse model
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Yi-Heng Tai1,*, Yu-Yi Lin1,*, Kai-Chen Wang2,*, Chao-Lin Chang3, Ru-Yin Chen3, Chia-Chu Wu3 and Irene H. Cheng1,4
1Institute of Brain Science, National Yang-Ming University, Taipei, Taiwan
2Department of Neurology, Cheng-Hsin General Hospital, Taipei, Taiwan
3Food Industry Research and Development Institute, Hsinchu, Taiwan
4Brain Research Center, National Yang-Ming University, Taipei, Taiwan
*These authors have contributed equally to this work
Irene H. Cheng, email: firstname.lastname@example.org
Keywords: Alzheimer’s disease; curcuminoid submicron particle; APP transgenic mouse; amyloid; curcumin
Received: August 29, 2017 Accepted: January 25, 2018 Published: January 31, 2018
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-D28k 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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