Department of Neurology, University of Texas Medical Branch, Galveston, TX 77555-0616, USA.
Curr Alzheimer Res. 2010 Feb;7(1):27-39. doi: 10.2174/156720510790274464.
Elevated amyloid-beta peptide (Abeta) and loss of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery of an Abeta - nAChR interaction, much effort has been expended to characterize the consequences of high versus low concentrations of Abeta on nAChRs. This review will discuss current knowledge on the subject at the molecular, cellular, and physiological levels with particular emphasis on understanding how Abeta - nAChR interaction may contribute to normal physiological processes as well as the etiology of AD.
淀粉样β肽（Abeta）升高和烟碱型乙酰胆碱受体（nAChRs）丧失在阿尔茨海默病（AD）的发病机制中尤为突出。自发现 Abeta-nAChR 相互作用以来，人们已经付出了很大的努力来描述 Abeta 高浓度与低浓度对 nAChRs 的影响。本综述将在分子、细胞和生理水平上讨论该主题的现有知识，特别强调了解 Abeta-nAChR 相互作用如何有助于正常生理过程以及 AD 的发病机制。
