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

β-Amyloid (Aβ) can form aggregates through self-assembly and produce neurotoxicity in the early stage of Alzheimer’s disease (AD). Therefore, the inhibition of Aβ assembly is considered as the primary target for AD therapy. In this study, we reported that fucoxanthin, a marine carotenoid, potently r...

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Bibliographic Details
Published in:	Journal of agricultural and food chemistry Vol. 65; no. 20; pp. 4092 - 4102
Main Authors:	Xiang, Siying, Liu, Fufeng, Lin, Jiajia, Chen, Huixin, Huang, Chunhui, Chen, Liping, Zhou, Yiying, Ye, Luying, Zhang, Ke, Jin, Jiukai, Zhen, Jiacheng, Wang, Chuang, He, Shan, Wang, Qinwen, Cui, Wei, Zhang, Jinrong
Format:	Journal Article
Language:	English
Published:	United States American Chemical Society 24-05-2017
Subjects:	Alzheimer Disease - drug therapy Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - psychology Amyloid beta-Peptides - chemistry Amyloid beta-Peptides - metabolism Animals Brain-Derived Neurotrophic Factor - genetics Brain-Derived Neurotrophic Factor - metabolism Cell Survival - drug effects Cognition - drug effects Hippocampus - drug effects Hippocampus - metabolism Humans Male Mice Mice, Inbred ICR Molecular Docking Simulation Neurons - drug effects Neurons - metabolism Xanthophylls - administration & dosage Alzheimer’s disease marine carotenoid fucoxanthin neuroprotection β-amyloid
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Summary:	β-Amyloid (Aβ) can form aggregates through self-assembly and produce neurotoxicity in the early stage of Alzheimer’s disease (AD). Therefore, the inhibition of Aβ 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 Aβ fibrils and oligomers. Moreover, the fucoxanthin-triggered modification significantly reduced the neurotoxicity of Aβ oligomers in vitro. Molecular dynamics simulation analysis further revealed a hydrophobic interaction between fucoxanthin and Aβ peptide, which might prevent the conformational transition and self-assembly of Aβ. Most importantly, fucoxanthin could attenuate cognitive impairments in Aβ 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 Aβ assembly and attenuating Aβ neurotoxicity.
ISSN:	0021-8561 1520-5118
DOI:	10.1021/acs.jafc.7b00805