期刊
NEUROTHERAPEUTICS
卷 7, 期 4, 页码 354-365出版社
SPRINGER
DOI: 10.1016/j.nurt.2010.05.014
关键词
Microglia; inflammation-mediated; neurodegeneration; oxidative stress; chronic neurotoxicity; reactive microgliosis
资金
- NIEHS/NIH [R00ES01549, R01ES016951]
- Institute for the Study of Aging/Alzheimer's Drug Discovery Foundation
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES016951] Funding Source: NIH RePORTER
Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurodegenerative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-alpha, nitric oxide, interleukin-1 beta, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson's disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据