首页> 美国卫生研究院文献>Translational Neurodegeneration >Constipation deficit in colon contractions and alpha-synuclein inclusions within the colon precede motor abnormalities and neurodegeneration in the central nervous system in a mouse model of alpha-synucleinopathy
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Constipation deficit in colon contractions and alpha-synuclein inclusions within the colon precede motor abnormalities and neurodegeneration in the central nervous system in a mouse model of alpha-synucleinopathy

机译:在小鼠α-突触核蛋白病模型中便秘结肠收缩不足和结肠内的α-突触核蛋白包涵体先于运动异常和中枢神经系统中的神经变性

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摘要

BackgroundGastrointestinal dysfunction can affect Parkinson’s disease (PD) patients long before the onset of motor symptoms. However, little is known about the relationship between gastrointestinal abnormalities and the development of PD. Contrary to other animal models, the human A53T alpha-synuclein (αS) transgenic mice, Line G2–3, develops αS-driven neurological and motor impairments after 9 months of age, displaying a long presymptomatic phase free of central nervous system (CNS) dysfunction.
机译:背景:胃肠功能障碍会在运动症状发作之前很久就影响帕金森氏病(PD)患者。然而,关于胃肠道异常与PD发展之间的关系知之甚少。与其他动物模型相反,人类A53Tα-突触核蛋白(αS)转基因小鼠G2–3系在9个月大后发展为αS驱动的神经和运动障碍,表现出无中枢神经系统(CNS)的较长的症状前期。功能障碍。

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