Air pollution: mechanisms of neuroinflammation and CNS disease.

Air pollution: mechanisms of neuroinflammation and CNS disease.
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DOI:
10.1016/j.tins.2009.05.009
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发表时间:
2009-09
影响因子:
15.9
通讯作者:
Calderon-Garciduenas, Lilian
Calderon-Garciduenas, Lilian
中科院分区:
医学1区
文献类型:
--
作者:
Block, Michelle L.;Calderon-Garciduenas, Lilian

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新出现的证据表明,空气污染是神经炎症、活性氧(ROS)和神经病理学的慢性来源,可引发中枢神经系统(CNS)疾病。中风发病率、阿尔茨海默病和帕金森病的病理学都与空气污染有关。最近的报告显示,空气污染成分会到达大脑。此外,已知影响肺和心血管疾病的全身效应也影响CNS健康。虽然驱动空气污染诱导的CNS病理学的机制知之甚少,但新的证据表明,小胶质细胞的激活和血脑屏障的变化可能是这一过程的关键。在这里,我们总结了最近的研究结果,详细说明了空气污染到达大脑并激活居民先天免疫反应的机制,成为促炎因子和ROS的慢性来源,这些因子和ROS可导致CNS疾病。
Emerging evidence implicates air pollution as a chronic source of neuroinflammation, reactive oxygen species (ROS), and neuropathology instigating central nervous system (CNS) disease. Stroke incidence, and Alzheimer’s and Parkinson’s disease pathology are linked to air pollution. Recent reports reveal that air pollution components reach the brain. Further, systemic effects known to impact lung and cardiovascular disease also impinge upon CNS health. While mechanisms driving air pollution-induced CNS pathology are poorly understood, new evidence suggests that activation of microglia and changes in the blood brain barrier may be key to this process. Here, we summarize recent findings detailing the mechanisms through which air pollution reaches the brain and activates the resident innate immune response to become a chronic source of pro-inflammatory factors and ROS culpable in CNS disease.
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