医学翻译——Aβ毒性研究新发现

原文：

The traditional “Aβ concept” is that Aβ induces neurotoxicity and cholinergic neuronal degeneration, in turn causing synaptic impairment, and learning and memory deficits53-55. However, emerging evidence shows that hAPP mice have epileptic seizures and synaptic and behavioral impairment without clear neuronal loss. Based on these findings, it has been proposed that Aβ-induced synaptic depression may result from a “homeostasis mechanism” involving neural adaptation in response to Aβ action19. For example, synaptic impairment may reflect compensation for Aβ-induced neural hyperexcitation. This homeostasis mechanism applies at many different levels, from receptors to circuits and networks. The proposed project will test this new concept by determining whether there is α7-nAChR adaptive alteration (numerical and/or functional upregulation) triggered by Aβ, and whether up-regulated α7-nAChRs contribute to Aβ-induced neural hyperexcitation.

译文：
传统观念认为，Aβ 可诱导神经毒性及胆碱能神经元变性，进而导致突触受损及学习、记忆缺陷53-55。然而，大量研究证实，在无明确神经元损伤的情况下，hAPP小鼠出现癫痫发作、突触损伤及行为损伤。因此，研究认为Aβ诱导的突触受损可能源于一种动态平衡机制，这种动态平衡与Aβ应激下的神经适应相关。 例如，突触受损可能为Aβ诱导的神经元兴奋过度的一种代偿性反应。该动态平衡机制适用于不同水平，如受体、神经元闭合回路及网络。本项目旨在验证是否存在Aβ引发的α7-nAChR适应性调节（表达或功能正向调节），及α7-nAChR上调能否引发Aβ诱导的神经元过度兴奋。