摘要
背景:阿尔茨海默病,一种神经变性疾病,其特征在于淀粉样蛋白β(Aβ)斑块,神经原纤维缠结和胆碱能神经元丧失的积累。 文献综述:Aβ斑块特别是胆碱能神经元丰富区域的定位已经导致Aβ以非常高的亲和力结合α7烟碱乙酰胆碱受体(nAChRs)。这一发现导致了这种结合的可能结果被广泛探索,从亚细胞信号传导途径到其对行为和认知功能的影响。有趣的是,有很多有关这种Aβ和α7nAChR相互作用的影响的冲突报道;一些研究报告了这种相互作用的神经保护作用,而另一些研究报告说它是神经毒性的。 结论:本文综述了Aβ和α7nAChR相互作用的神经毒性和神经保护作用及其对不同细胞信号通路和其他生理功能的影响。此外,这种相互作用可能对阿尔茨海默病治疗的影响也进行了讨论。
关键词: 阿尔茨海默病,α7烟碱受体,Aβ肽,胆碱能,神经保护,神经毒性。
Current Drug Targets
Title:Neuroprotective and Neurotoxic Implications of α7 Nicotinic Acetylcholine Receptor and Aβ Interaction: Therapeutic Options in Alzheimer's Disease
Volume: 18 Issue: 13
关键词: 阿尔茨海默病,α7烟碱受体,Aβ肽,胆碱能,神经保护,神经毒性。
摘要: Background: Alzheimer's disease, a neurodegenerative disorder, is characterized by accumulation of amyloid beta (Aβ) plaques, neurofibrillary tangles and loss of cholinergic neurons.
Literature review: The localization of Aβ plaques particularly in the cholinergic neuron-rich areas has led to the discovery that Aβ binds to α7 nicotinic acetylcholine receptors (nAChRs) with very high affinity. This discovery has led to extensive exploration of the possible outcomes of this binding, ranging from the subcellular signaling pathways to its effects on behavioral and cognitive functions. Intriguingly, there are conflicting reports about the effects of this Aβ and α7 nAChR interaction; a few studies report a neuroprotective role of this interaction while others claim that it is neurotoxic. Conclusion: This review focuses on the neurotoxic and neuroprotective effects of Aβ and α7 nAChR interaction and its implications on different cell signaling pathways and other physiological functions. Moreover, the implications this interaction might have on Alzheimer's disease therapy are also discussed.Export Options
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Cite this article as:
Neuroprotective and Neurotoxic Implications of α7 Nicotinic Acetylcholine Receptor and Aβ Interaction: Therapeutic Options in Alzheimer's Disease, Current Drug Targets 2017; 18 (13) . https://dx.doi.org/10.2174/1389450117666161005145143
DOI https://dx.doi.org/10.2174/1389450117666161005145143 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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