Abstract

Parkinson’s disease (PD) is thought to be caused by a combination of genetic and environmental factors. Bacterial or viral infection has been proposed as a potential risk factor, and there is supporting although not entirely consistent epidemiologic and basic science evidence to support its role. Encephalitis caused by influenza has included parkinsonian features. Epidemiological evidence is most compelling for an association between PD and hepatitis C virus. Infection with Helicobacter pylori may be associated not only with PD risk but also response to levodopa. Rapidly evolving knowledge regarding the role of the microbiome also suggests a role of resident bacteria in PD risk. Biological plausibility for the role for infectious agents is supported by the known neurotropic effects of specific viruses, particular vulnerability of the substantia nigra and even the promotion of aggregation of alpha-synuclein. A common feature of implicated viruses appears to be production of high levels of cytokines and chemokines that can cross the blood-brain barrier leading to microglial activation and inflammation and ultimately neuronal cell death. Based on multiple avenues of evidence it appears likely that specific bacterial and particularly viral infections may increase vulnerability to PD. The implications of this for PD prevention requires attention and may be most relevant once preventive treatments for at-risk populations are developed.

中文翻译：

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帕金森病的感染和风险

摘要

帕金森病 (PD) 被认为是由遗传和环境因素共同引起的。细菌或病毒感染被认为是一个潜在的危险因素，并且有支持其作用的流行病学和基础科学证据，尽管并不完全一致。流感引起的脑炎包括帕金森病的特征。流行病学证据最令人信服地证明 PD 与丙型肝炎病毒之间存在关联。感染幽门螺杆菌可能不仅与 PD 风险有关，而且与对左旋多巴的反应有关。关于微生物组作用的快速发展的知识也表明常驻细菌在 PD 风险中的作用。特定病毒的已知嗜神经作用、黑质的特别脆弱性，甚至促进 α-突触核蛋白的聚集，都支持了传染原作用的生物学合理性。相关病毒的一个共同特征似乎是产生高水平的细胞因子和趋化因子，这些细胞因子和趋化因子可以穿过血脑屏障，导致小胶质细胞激活和炎症，最终导致神经元细胞死亡。基于多种途径的证据，似乎特定的细菌和特别是病毒感染可能会增加对 PD 的易感性。