Curcuminoid submicron particle ameliorates cognitive deficits and decreases amyloid pathology in Alzheimer's disease mouse model.

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 and better neuroprotective effect against oligomeric Aβ than un-nanosized curcuminoids . Two months of CSP consumption reversed spatial memory deficits and the loss of a calcium binding protein calbindin-D in the hippocampus of AD mouse model. In addition, CSP consumption lowered amyloid plaques and astrogliosis and enhanced microglial Aβ phagocytosis , 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.