Baizabal-Carvallo José Fidel, Alonso-Juarez Marlene
Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX, USA; University of Guanajuato, Mexico.
National Polytechnique Institute, Mexico City, Mexico.
Neuroscience. 2020 Apr 15;432:160-173. doi: 10.1016/j.neuroscience.2020.02.030. Epub 2020 Feb 27.
Parkinson's disease (PD) is the second most common neurodegenerative disorder. Despite its high frequency the etiology is still unclear; several lines of evidence show that an inflammatory process is implicated in the pathogenesis of this disorder; where activation of brain microglia plays a central role in the damage of dopaminergic neurons of the substantia nigra. Such inflammation has been attributed to the toxic effect of aggregated α-synuclein; however, evidence also implicates an altered gut microbiota (dysbiosis) through the systemic release of endotoxins such as lipopolysaccharide and other metabolic products. This exposure may be enhanced by increased permeability of the intestinal ("leaky gut") and the blood brain barrier; enhancing the entrance of microbiota-produced substances into the central nervous system. In this manuscript, we explore the evidence from clinical and basic science implicating microglia activation by gut dysbiosis and how this phenomenon may impact in the symptomatology and progression of PD.
帕金森病（PD）是第二常见的神经退行性疾病。尽管其发病率很高，但其病因仍不清楚；多项证据表明，炎症过程与该疾病的发病机制有关；其中脑小胶质细胞的激活在黑质多巴胺能神经元的损伤中起核心作用。这种炎症被归因于聚集的α-突触核蛋白的毒性作用；然而，证据也表明肠道微生物群改变（生态失调）通过脂多糖等内毒素和其他代谢产物的全身释放而起作用。肠道（“肠漏”）和血脑屏障通透性增加可能会增强这种暴露，从而增加微生物产生的物质进入中枢神经系统的机会。在本手稿中，我们探讨了临床和基础科学中关于肠道生态失调导致小胶质细胞激活的证据，以及这种现象如何影响帕金森病的症状和进展。
