What Is Our Understanding of the Influence of Gut Microbiota on the Pathophysiology of Parkinson's Disease?
What Is Our Understanding of the Influence of Gut Microbiota on the Pathophysiology of Parkinson's Disease?
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DOI：
10.3389/fnins.2021.708587
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发表时间：
2021
影响因子：
4.3
通讯作者：
Burnet PWJ
中科院分区：
文献类型：
--
作者：
Hill AE;Wade-Martins R;Burnet PWJ
微生物群越来越多地与人类疾病的易感性有关，包括神经退行性疾病，如帕金森病（PD）。传统上，以中枢神经系统（CNS）为中心的方法来理解PD占主导地位;然而，自从帕金森自己报告了这种疾病以来，肠道与PD的关系就一直存在。肠脑轴是指胃肠道（GIT）和大脑之间的双向通信。在PD患者中报告的肠道微生物群失调可能将其扩展到微生物群-肠道-脑轴。迄今为止，主要研究了细菌组。假设伴随生态失调的细菌产物丰度的变化通过多种机制影响PD病理生理学，这些机制广泛集中于炎症，这是α-突触核蛋白（α-syn）错误折叠的原因。假设肠道微生物群可以影响PD病理生理学的两个主要途径，即神经和体液途径。神经途径涉及肠神经中的a-syn外周错误折叠，然后可以通过迷走神经将其运输到大脑。体液途径涉及细菌产物和促炎细胞因子从肠道经由循环的运输，其可通过诱导神经炎症引起中枢a-syn错误折叠。本文将评估当前文献是否支持肠道细菌通过两种途径影响PD病理生理学。
Microbiota have increasingly become implicated in predisposition to human diseases, including neurodegenerative disorders such as Parkinson’s disease (PD). Traditionally, a central nervous system (CNS)-centric approach to understanding PD has predominated; however, an association of the gut with PD has existed since Parkinson himself reported the disease. The gut–brain axis refers to the bidirectional communication between the gastrointestinal tract (GIT) and the brain. Gut microbiota dysbiosis, reported in PD patients, may extend this to a microbiota–gut–brain axis. To date, mainly the bacteriome has been investigated. The change in abundance of bacterial products which accompanies dysbiosis is hypothesised to influence PD pathophysiology via multiple mechanisms which broadly centre on inflammation, a cause of alpha-synuclein (a-syn) misfolding. Two main routes are hypothesised by which gut microbiota can influence PD pathophysiology, the neural and humoral routes. The neural route involves a-syn misfolding peripherally in the enteric nerves which can then be transported to the brain via the vagus nerve. The humoral route involves transportation of bacterial products and proinflammatory cytokines from the gut via the circulation which can cause central a-syn misfolding by inducing neuroinflammation. This article will assess whether the current literature supports gut bacteria influencing PD pathophysiology via both routes.
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