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胆固醇、脂质、淀粉样β和阿尔茨海默病。

Cholesterol, lipids, amyloid Beta, and Alzheimer's.

机构信息

Japan Advanced Institute of Science and Technology, Nomi City, Ishikawa, Japan.

出版信息

Curr Alzheimer Res. 2010 May;7(3):262-70. doi: 10.2174/156720510791050821.

DOI:10.2174/156720510791050821
PMID:19715550
Abstract

High levels of cholesterol have been proposed as a risk factor for Alzheimer's disease (AD). Polymorphism of genes encoding proteins that regulate cholesterol metabolism have also been associated with the frequency of Alzheimer's development. Some studies have shown that cholesterol-lowering drugs reduce the frequency of AD development. The proposed role of cholesterol in AD has been challenged by several studies. In this review, we provide a brief account of the major pieces of evidence in support of and against the possible role of cholesterol in the development of AD, and the methodologies used. We highlight the interactions between cholesterol and amyloid beta (Abeta) and, with the peptide's precursor protein. Drawing from our teams' recent findings, we speculate on how Abeta peptides may influence the fluidity, stability of the membrane, as well as membrane morphological changes.

摘要

胆固醇水平升高被认为是阿尔茨海默病(AD)的一个风险因素。调节胆固醇代谢的蛋白质的基因多态性也与阿尔茨海默病的发病频率有关。一些研究表明,降低胆固醇的药物可以降低 AD 发病的频率。胆固醇在 AD 中的作用受到了一些研究的质疑。在这篇综述中,我们简要介绍了支持和反对胆固醇在 AD 发展中可能作用的主要证据,以及所使用的方法。我们强调了胆固醇与淀粉样蛋白β(Abeta)之间的相互作用,以及与肽的前体蛋白之间的相互作用。根据我们团队的最新发现,我们推测 Abeta 肽如何影响膜的流动性、稳定性以及膜形态的变化。

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Cholesterol, lipids, amyloid Beta, and Alzheimer's.胆固醇、脂质、淀粉样β和阿尔茨海默病。
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2
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