Cholesterol, lipids, amyloid Beta, and Alzheimer's.
Cholesterol, lipids, amyloid Beta, and Alzheimer's.
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DOI：
10.2174/156720510791050821
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发表时间：
2010-05
影响因子：
2.1
通讯作者：
Mun'delanji C. Vestergaard;T. Hamada;Masamune Morita;M. Takagi
中科院分区：
文献类型：
--
作者：
Mun'delanji C. Vestergaard;T. Hamada;Masamune Morita;M. Takagi
高胆固醇水平已被认为是阿尔茨海默病 (AD) 的危险因素。编码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生频率有关。一些研究表明，降胆固醇药物可以降低 AD 发生的频率。胆固醇在 AD 中的作用已受到多项研究的质疑。在这篇综述中，我们简要介绍了支持和反对胆固醇在 AD 发展中可能发挥作用的主要证据以及所使用的方法。我们强调胆固醇和β淀粉样蛋白（Abeta）之间以及与肽前体蛋白之间的相互作用。根据我们团队最近的发现，我们推测 Abeta 肽如何影响膜的流动性、稳定性以及膜形态变化。
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.