Department of Anatomy and Cell Biology, The Stark Neuroscience Research Institute, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Department of Environmental Health, Indiana University Richard M. Fairbanks School of Public Health, Indiana University, Indianapolis, IN, 46202, USA.
Curr Environ Health Rep. 2017 Jun;4(2):166-179. doi: 10.1007/s40572-017-0142-3.
Accumulating research indicates that ambient outdoor air pollution impacts the brain and may affect neurodegenerative diseases, yet the potential underlying mechanisms are poorly understood.
The neuroinflammation hypothesis holds that elevation of cytokines and reactive oxygen species in the brain mediates the deleterious effects of urban air pollution on the central nervous system (CNS). Studies in human and animal research document that neuroinflammation occurs in response to several inhaled pollutants. Microglia are a prominent source of cytokines and reactive oxygen species in the brain, implicated in the progressive neuron damage in diverse neurodegenerative diseases, and activated by inhaled components of urban air pollution through both direct and indirect pathways. The MAC1-NOX2 pathway has been identified as a mechanism through which microglia respond to different forms of air pollution, suggesting a potential common deleterious pathway. Multiple direct and indirect pathways in response to air pollution exposure likely interact in concert to exert CNS effects.
越来越多的研究表明，环境室外空气污染会影响大脑，并可能影响神经退行性疾病，但潜在的机制尚不清楚。
神经炎症假说认为，大脑中细胞因子和活性氧的升高介导了城市空气污染对中枢神经系统（CNS）的有害影响。人类和动物研究的研究记录表明，神经炎症是对几种吸入污染物的反应。小胶质细胞是大脑中细胞因子和活性氧的主要来源，与多种神经退行性疾病中的进行性神经元损伤有关，并通过直接和间接途径被城市空气污染的吸入成分激活。MAC1-NOX2 途径已被确定为小胶质细胞对不同形式空气污染作出反应的一种机制，这表明存在一种潜在的共同有害途径。可能有多种直接和间接的途径对空气污染暴露作出反应，共同发挥中枢神经系统的作用。
