Perez-Pardo Paula, Hartog Mitch, Garssen Johan, Kraneveld Aletta D
Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands.
Nutricia Research, Utrecht, The Netherlands.
Curr Behav Neurosci Rep. 2017;4(4):361-368. doi: 10.1007/s40473-017-0129-2. Epub 2017 Nov 8.
Patients suffering from Parkinson's disease (PD) are known to experience gastrointestinal dysfunction that might precede the onset of motor symptoms by several years. Evidence suggests an important role of the gut-brain axis in PD pathogenesis. These interactions might be essentially influenced by the gut microbiota. Here, we review recent findings supporting that changes in the gut microbiota composition might be a trigger for inflammation contributing to neurodegeneration in PD.
Recent research revealed that PD patients exhibit a pro-inflammatory microbiota profile in their intestinal tract that might increase gut permeability, allowing leakage of bacterial products and inflammatory mediators from the intestines. Evidence in literature indicates that alpha-synuclein deposition might start in the enteric nervous system by pro-inflammatory immune activity and then propagates to the CNS. Alternatively, the peripheral inflammatory response could impact the brain through systemic mechanisms.
A better understanding of the gut-brain interactions and the role of the intestinal microbiota in the regulation of immune responses might bring new insights in PD pathological progression and might lead to novel diagnostics and therapeutic approaches.
已知帕金森病（PD）患者会出现胃肠功能障碍，这种障碍可能在运动症状出现前数年就已存在。有证据表明，肠-脑轴在PD发病机制中起重要作用。这些相互作用可能主要受肠道微生物群影响。在此，我们综述近期的研究发现，这些发现支持肠道微生物群组成的变化可能是导致PD神经退行性变的炎症触发因素。
近期研究表明，PD患者肠道内呈现促炎微生物群特征，这可能会增加肠道通透性，使细菌产物和炎症介质从肠道渗漏。文献证据表明，α-突触核蛋白沉积可能通过促炎免疫活动在肠神经系统开始，然后扩散至中枢神经系统。或者，外周炎症反应可能通过全身机制影响大脑。
更好地理解肠-脑相互作用以及肠道微生物群在免疫反应调节中的作用，可能为PD病理进展带来新见解，并可能导致新的诊断和治疗方法。
