{"title":"Human gut microbiota and Parkinson Disease","authors":"M. Güzel","doi":"10.37212/jcnos.610152","DOIUrl":null,"url":null,"abstract":"Human gut microbiota (GM) has now been accepted as a potential modulator ofhuman biology. Although new to the world of science, GM's impaction brain and behavior has drawn great attention around the globe. Studies have now proven that GM can directly or indirectly modify brain neurochemistry via various mechanisms like neural, immune and endocrine. The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. This presentation is an overview of recent findings regarding the GM -brain axis in PD (Braniste et al. 2014; Sampson et al. 2016) Parkinson disease (PD) is the second-most common neurodegenerative disorder. PD patients show alpha-synuclein deposits and neurodegeneration in the enteric nervous system as well as breakdown of the mucosal barrier, bacterial invasion, and mucosal inflammation in the colon. Alterations in GM and increased gut permeability may influence PD pathophysiology via epigenetic processes that alter αSyn regulation (Matsumoto et al. 2010). Sampson et al. (2016) suggest that GM are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. They propose that GM regulate movement disorders and suggest that alterations in the human microbiome represent a risk factor for PD. GM do not only affect gut physiology, but there is also an intense bidirectional interaction with the brain influencing neuronal activity, behavior, as well as levels of neurotransmitter receptors, neurotrophic factors, and inflammation. Recently, gut microbiome alterations in PD subjects and a connection between GM and motoras well as non-motor symptoms have been described (Sampson et al. 2016; Parashar and Udayabanu 2017)","PeriodicalId":37782,"journal":{"name":"Journal of Cellular Neuroscience and Oxidative Stress","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2018-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cellular Neuroscience and Oxidative Stress","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.37212/jcnos.610152","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Biochemistry, Genetics and Molecular Biology","Score":null,"Total":0}
引用次数: 0
Abstract
Human gut microbiota (GM) has now been accepted as a potential modulator ofhuman biology. Although new to the world of science, GM's impaction brain and behavior has drawn great attention around the globe. Studies have now proven that GM can directly or indirectly modify brain neurochemistry via various mechanisms like neural, immune and endocrine. The intestinal microbiota influence neurodevelopment, modulate behavior, and contribute to neurological disorders. This presentation is an overview of recent findings regarding the GM -brain axis in PD (Braniste et al. 2014; Sampson et al. 2016) Parkinson disease (PD) is the second-most common neurodegenerative disorder. PD patients show alpha-synuclein deposits and neurodegeneration in the enteric nervous system as well as breakdown of the mucosal barrier, bacterial invasion, and mucosal inflammation in the colon. Alterations in GM and increased gut permeability may influence PD pathophysiology via epigenetic processes that alter αSyn regulation (Matsumoto et al. 2010). Sampson et al. (2016) suggest that GM are required for the hallmark motor and GI dysfunction in a mouse model of PD, via postnatal gut-brain signaling by microbial molecules that impact neuroinflammation and αSyn aggregation. They propose that GM regulate movement disorders and suggest that alterations in the human microbiome represent a risk factor for PD. GM do not only affect gut physiology, but there is also an intense bidirectional interaction with the brain influencing neuronal activity, behavior, as well as levels of neurotransmitter receptors, neurotrophic factors, and inflammation. Recently, gut microbiome alterations in PD subjects and a connection between GM and motoras well as non-motor symptoms have been described (Sampson et al. 2016; Parashar and Udayabanu 2017)
人类肠道菌群(GM)现已被认为是人类生物学的潜在调节剂。虽然转基因对科学界来说是一个新事物,但它对大脑和行为的影响已经引起了全球的极大关注。目前已有研究证明转基因可以通过神经、免疫、内分泌等多种机制直接或间接地改变脑神经化学。肠道微生物群影响神经发育,调节行为,并有助于神经系统疾病。本报告概述了PD中GM -脑轴的最新发现(Braniste et al. 2014;Sampson et al. 2016)帕金森病(PD)是第二常见的神经退行性疾病。PD患者表现为-突触核蛋白沉积和肠神经系统神经退行性变,以及粘膜屏障破坏、细菌侵袭和结肠粘膜炎症。GM的改变和肠道通透性的增加可能通过改变α - syn调节的表观遗传过程影响PD的病理生理(Matsumoto et al. 2010)。Sampson等人(2016)认为,通过影响神经炎症和αSyn聚集的微生物分子在出生后的肠-脑信号传导,转基因是PD小鼠模型中标志性的运动和GI功能障碍所必需的。他们提出转基因调节运动障碍,并提出人类微生物组的改变是帕金森病的一个危险因素。转基因不仅影响肠道生理,而且还与大脑产生强烈的双向相互作用,影响神经元活动、行为以及神经递质受体、神经营养因子和炎症的水平。最近,研究人员描述了PD患者肠道微生物组的改变以及GM与运动和非运动症状之间的联系(Sampson等人,2016;Parashar and Udayabanu 2017)
期刊介绍:
Journal of Cellular Neuroscience and Oxidative Stress isan online journal that publishes original research articles, reviews and short reviews on themolecular basisofbiophysical,physiological and pharmacological processes thatregulate cellular function, and the control or alteration of these processesby theaction of receptors, neurotransmitters, second messengers, cation, anions,drugsor disease. Areas of particular interest are four topics. They are; 1. Ion Channels (Na+-K+Channels, Cl– channels, Ca2+channels, ADP-Ribose and metabolism of NAD+,Patch-Clamp applications) 2. Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) 3. Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD+ on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson’s and Alzheimer’s diseases) 4. Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)