Dineley Kelly T
Department of Neurology, George and Cynthia Mitchell Research Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX 77555-0874, USA.
Front Biosci. 2007 Sep 1;12:5030-8. doi: 10.2741/2445.
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 understand how this interaction may contribute to normal physiological processes as well as AD. Several researchers have expanded on the initial observation of an Abeta-nAChR interaction to characterize the pertinent factors that confer Abeta sensitivity to nAChRs. Some of which include the following: 1. receptor subunit composition; 2. receptor subunit stoichiometry; 3. regional distribution; 4. presynaptic versus somatic distribution; 5. neuron versus glia expression; 6. in vitro expression system. These aspects of nAChR composition and expression appear to confer the specific functional consequences of Abeta interaction which range from blockade of receptor activation to stimulation of second messenger cascades that provide neuroprotection from Abeta toxicity. This review will discuss the extant literature on the subject in terms of clarifying this apparent dichotomy regarding the consequences of Abeta-nAChR interaction during health and disease.
淀粉样β肽（Aβ）水平升高和烟碱型乙酰胆碱受体（nAChRs）丧失在阿尔茨海默病（AD）的病因中显著存在。自从发现Aβ与nAChR相互作用以来，人们付出了很多努力来了解这种相互作用如何影响正常生理过程以及AD。几位研究人员在最初观察到的Aβ与nAChR相互作用的基础上进行了拓展，以确定赋予nAChRs对Aβ敏感性的相关因素。其中一些因素包括：1. 受体亚基组成；2. 受体亚基化学计量；3. 区域分布；4. 突触前与体细胞分布；5. 神经元与胶质细胞表达；6. 体外表达系统。nAChR组成和表达的这些方面似乎赋予了Aβ相互作用的特定功能后果，范围从受体激活的阻断到第二信使级联反应的刺激，从而提供对Aβ毒性的神经保护。本综述将讨论关于该主题的现有文献，以阐明在健康和疾病状态下Aβ与nAChR相互作用后果方面明显的二分法。
