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从神经科学角度看帕金森病的“肠源性”理论。

A neuroscience perspective of the gut theory of Parkinson's disease.

机构信息

Department of Anatomy, Brain Health Research Centre, and Brain Research New Zealand, University of Otago, PO Box 913, Dunedin, 9054, New Zealand.

出版信息

Eur J Neurosci. 2019 Mar;49(6):817-823. doi: 10.1111/ejn.13869. Epub 2018 Feb 28.

DOI:10.1111/ejn.13869
PMID:29446158
Abstract

Parkinson's disease is caused by complex interactions between environmental factors and a genetic predisposition. Environmental factors include exposure to pesticides and toxins, heavy metals and accumulation of iron and/or manganese in the brain. However, accumulating evidence indicates that gut-brain health and function are impaired in Parkinson's disease, often a decade before motor symptoms are diagnosed. We present the gut-brain theory of Parkinson's disease and summarise the peripheral and central nervous system pathology, gastrointestinal symptoms experienced by many Parkinson's patients, the route by which gut-brain dysfunction may occur and changes in gut microbiota that are associated with disease expression. Finally, we consider future gut-based treatments to prevent or slow down the progression of Parkinson's disease and explore whether this knowledge may highlight biomarkers to be included in complex algorithms in the future to assess a person's risk of developing Parkinson's disease.

摘要

帕金森病是由环境因素和遗传易感性之间的复杂相互作用引起的。环境因素包括接触杀虫剂和毒素、重金属以及大脑中铁和/或锰的积累。然而,越来越多的证据表明,帕金森病患者的肠道-大脑健康和功能受损,通常在运动症状被诊断出前十年就已经出现。我们提出了帕金森病的肠-脑理论,并总结了外周和中枢神经系统病理学、许多帕金森病患者经历的胃肠道症状、肠道-大脑功能障碍可能发生的途径以及与疾病表达相关的肠道微生物组的变化。最后,我们考虑了未来基于肠道的治疗方法来预防或减缓帕金森病的进展,并探讨了这些知识是否可以突出未来用于评估个体患帕金森病风险的复杂算法中包含的生物标志物。

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