帕金森病中的神经炎症。
Neuroinflammation in Parkinson's disease.
机构信息
Department of Physiology, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
出版信息
J Neuroimmune Pharmacol. 2009 Dec;4(4):419-29. doi: 10.1007/s11481-009-9176-0. Epub 2009 Oct 10.
Abstract
During the last two decades, a wealth of animal and human studies has implicated inflammation-derived oxidative stress and cytokine-dependent neurotoxicity in the progressive degeneration of the dopaminergic nigrostriatal pathway, the hallmark of Parkinson's disease (PD). In this review, we discuss the various hypotheses regarding the role of microglia and other immune cells in PD pathogenesis and progression, the inflammatory mechanisms implicated in disease progression from pre-clinical and clinical studies, the recent evidence that systemic inflammation can trigger microglia activation in PD-relevant central nervous system regions, the synergism between gene products linked to parkinsonian phenotypes (alpha-synuclein, parkin, Nurr1, and regulator of G-protein signaling-10) and neuroinflammation in promoting neurodegeneration of the nigrostriatal pathway, and the latest update on meta-analysis of epidemiological studies on the risk-lowering effects of anti-inflammatory drug regimens.
摘要
在过去的二十年中，大量的动物和人体研究表明，炎症引起的氧化应激和细胞因子依赖性神经毒性与多巴胺能黑质纹状体通路的进行性退化有关，这是帕金森病（PD）的标志。在这篇综述中，我们讨论了关于小胶质细胞和其他免疫细胞在 PD 发病机制和进展中的作用的各种假说，从临床前和临床研究中涉及疾病进展的炎症机制，最近的证据表明全身炎症可以触发与 PD 相关的中枢神经系统区域中小胶质细胞的激活，与帕金森病表型相关的基因产物（α-突触核蛋白、parkin、Nurr1 和 G 蛋白信号调节因子 10）与神经炎症之间的协同作用促进黑质纹状体通路的神经退行性变，以及对抗炎药物方案降低风险的流行病学研究的荟萃分析的最新更新。
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