The First Affiliated Hospital/Zhengzhou University, Zhengzhou, China; Biological Psychiatry International Joint Laboratory of Henan/Zhengzhou University, Zhengzhou, China; Henan Psychiatric Transformation Research Key Laboratory/Zhengzhou University, Zhengzhou, China.
Department of Biomedical Engineering, College of Engineering, Peking University, Beijing, China.
Biochem Biophys Res Commun. 2019 Apr 30;512(2):373-380. doi: 10.1016/j.bbrc.2019.02.152. Epub 2019 Mar 18.
Schizophrenia is a severe mental disorder with unknown etiology. Many mechanisms, including dysregulation of neurotransmitters, immune disturbance, and abnormal neurodevelopment, are proposed for the pathogenesis of schizophrenia. The significance of communication between intestinal flora and the central nervous system through the gut-brain axis is increasingly being recognized. The intestinal microbiota plays an important role in regulating neurotransmission, immune homeostasis, and brain development. We hypothesize that an imbalance in intestinal flora causes immune activation and dysfunction in the gut-brain axis, contributing to schizophrenia. In this review, we examine recent studies that explore the intestinal flora and immune-mediated neurodevelopment of schizophrenia. We conclude that an imbalance in intestinal flora may reduce protectants and increase neurotoxin and inflammatory mediators, causing neuronal and synaptic damage, which induces schizophrenia.
精神分裂症是一种病因不明的严重精神障碍。许多机制,包括神经递质失调、免疫紊乱和异常神经发育,被提出用于精神分裂症的发病机制。肠道菌群通过肠脑轴与中枢神经系统之间的交流的重要性越来越受到重视。肠道微生物群在调节神经传递、免疫稳态和大脑发育方面发挥着重要作用。我们假设肠道菌群失衡会导致免疫激活和肠脑轴功能障碍,从而导致精神分裂症。在这篇综述中,我们研究了最近探索精神分裂症肠道菌群和免疫介导的神经发育的研究。我们得出结论,肠道菌群失衡可能会减少保护因子,增加神经毒素和炎症介质,导致神经元和突触损伤,从而引发精神分裂症。