Fucoxanthin Inhibits β-Amyloid Assembly and Attenuates β-Amyloid Oligomer-Induced Cognitive Impairments

beta-Amyloid (A beta) can form aggregates through self-assembly and produce neurotoxicity in the early stage of Alzheimer's disease (AD). Therefore, the inhibition of A beta assembly is considered as the primary target for AD therapy. In this study, we reported that fucoxanthin, a marine carotenoid, potently reduced the formation of A beta fibrils and oligomers. Moreover, the fucoxanthin-triggered modification significantly reduced the neurotoxicity of A beta oligomers in vitro. Molecular dynamics simulation analysis further revealed a hydrophobic interaction between fucoxanthin and A beta peptide, which might prevent the conformational transition and self-assembly of A beta. Most importantly, fucoxanthin could attenuate cognitive impairments in A beta oligomer-injected mice. In addition, fucoxanthin significantly inhibited oxidative stress, enhanced the expression of brain-derived neurotrophic factor, and increased ChAT-positive regions in the hippocampus of mice. On the basis of these novel findings, we anticipated that fucoxanthin might ameliorate AD via inhibiting AP assembly and attenuating A beta neurotoxicity.