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首页> 外文期刊>中国药理学报：英文版 >Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate β-amyloid neurotoxicity
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Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate β-amyloid neurotoxicity

机译：神经元烟碱乙酰胆碱受体充当介导β淀粉样蛋白神经毒性的敏感靶标

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摘要

Alzheimer's disease (AD) is the most common form of brain dementia characterized by the accumulation of β-amyloid peptides (Aβ) and loss of forebrain cholinergic neurons. Aβ accumulation and aggregation are thought to contribute to cholinergic neuronal degeneration, in turn causing learning and memory deficits, but the specific targets that mediate Aβ neurotoxicity remain elusive. Recently, accumlating lines of evidence have demonstrated that Aβ directly modulates the function of neuronal nicotinic acetylcholine receptors (nAChRs), which leads to the new hypothesis that neuronal nAChRs may serve as important targets that mediate Aβ neurotoxicity. In this review, we summarize current studies performed in our laboratory and in others to address the question of how Aβ modulates neuronal nAChRs, especially nAChR subunit function.
机译：阿尔茨海默病（AD）是最常见的脑痴呆形式，其特征在于β-淀粉样肽（Aβ）的积累和前脑胆碱能神经元的丧失。据认为，Aβ积聚和聚集是有助于胆碱能神经元变性，反过来导致学习和记忆缺陷，但介导Aβ神经毒性的特定靶标仍然难以捉摸。最近，累积证据型已经证明Aβ直接调节神经元烟碱乙酰胆碱受体（NACHR）的功能，这导致新假设是神经元NACHRS可以作为介导Aβ神经毒性的重要靶标。在这篇综述中，我们总结了当前在我们的实验室和其他研究中进行的研究，以解决Aβ如何调节神经元NACHR的问题，特别是NACHR亚基功能。

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