帕金森病的新视角:探讨肠道和迷走神经裂解物在α-突触核蛋白病传播中的作用

R. Ullah, V. Dawson, T. Dawson
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引用次数: 0

摘要

在帕金森病(PD)中,错误折叠的α-突触核蛋白(α-syn)在大脑中的积累是该疾病的一个主要病理特征。α-Syn的形成和聚集可能起源于肠神经系统,病理性α-Syn可通过迷走神经传递到中枢神经系统。在这篇评论中,我们总结了Yang等人[1]的研究结果,他们报道了帕金森病患者含有病理性α-syn的肠道和迷走神经溶解物能够模版内源性大鼠α-syn,最终导致病理性α-syn的扩散、病理性α-syn的沉积、不同脑区神经炎症和多巴胺神经元的神经变性。这些观察结果与其他支持胃肠系统在PD发病机制中的重要性的研究进行了讨论,并强调了未来的研究方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A new Perspective on Parkinson's disease: exploring the involvement of intestine and vagus lysates in α-synucleinopathy propagation
In Parkinson's disease (PD), the accumulation of misfolded α-synuclein (α-syn) in the brain is a major characteristic of the pathology. α-Syn formation and aggregation may originate in the enteric nervous system and pathologic α-syn can be transmitted to the central nervous system via the vagus nerve. In this commentary, we summarize the findings of Yang et al.[1] in which they report on the ability of a Parkinson’s disease patient's intestinal and vagus lysates containing pathologic α-syn to template endogenous rat α-syn culminating in the spread of pathologic α-syn, deposition of pathologic α-syn, and neuroinflammation in different brain regions and neurodegeneration of dopamine neurons. These observations are discussed with other studies supporting the significance of the gastrointestinal system in PD pathogenesis and future directions of research are highlighted.
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