School of Life and Health Sciences, Aston University, Birmingham, UK.
Biochem Pharmacol. 2011 Oct 15;82(8):931-42. doi: 10.1016/j.bcp.2011.06.039. Epub 2011 Jul 7.
Aberrant amyloid-β peptide (Aβ) accumulation along with altered expression and function of nicotinic acetylcholine receptors (nAChRs) stand prominently in the etiology of Alzheimer's disease (AD). Since the discovery that Aβ is bound to α7 nAChRs under many experimental settings, including post-mortem AD brain, much effort has been expended to understand the implications of this interaction in the disease milieu. This research update will review the current literature on the α7 nAChR-Aβ interaction in vitro and in vivo, the functional consequences of this interaction from sub-cellular to cognitive levels, and discuss the implications these relationships might have for AD therapies.
淀粉样β肽（Aβ）的异常积累，以及烟碱型乙酰胆碱受体（nAChRs）的表达和功能改变，在阿尔茨海默病（AD）的发病机制中尤为突出。自从在许多实验环境下，包括死后 AD 大脑中发现 Aβ与α7 nAChR 结合以来，人们已经付出了很大的努力来理解这种相互作用在疾病环境中的意义。本研究更新将回顾α7 nAChR-Aβ相互作用在体外和体内的最新文献，从亚细胞到认知水平的这种相互作用的功能后果，并讨论这些关系对 AD 治疗可能具有的意义。
