在帕金森病A53T小鼠模型中,慢性隔离应激与结肠和运动症状增加有关

S. Diwakarla, D. Finkelstein, Remy Constable, O. Artaiz, M. D. Di Natale, R. McQuade, Enie Lei, Xin-Yi Chai, M. Ringuet, L. Fothergill, V. Lawson, L. Ellett, Joel P. Berger, J. Furness
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引用次数: 5

摘要

在几种帕金森病(PD)啮齿动物模型中,慢性应激加剧运动缺陷并增加多巴胺能细胞损失。然而,对于应激对胃肠功能障碍(PD的一种常见非运动症状)的影响知之甚少。我们的目的是确定慢性应激是否会加剧A53T PD小鼠模型的胃肠道功能障碍,以及这是否与α‐突触核蛋白分布的变化有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic isolation stress is associated with increased colonic and motor symptoms in the A53T mouse model of Parkinson’s disease
Chronic stress exacerbates motor deficits and increases dopaminergic cell loss in several rodent models of Parkinson's disease (PD). However, little is known about effects of stress on gastrointestinal (GI) dysfunction, a common non‐motor symptom of PD. We aimed to determine whether chronic stress exacerbates GI dysfunction in the A53T mouse model of PD and whether this relates to changes in α‐synuclein distribution.
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