Inflammation and neurodegeneration in Parkinson's disease
Inflammation and neurodegeneration in Parkinson's disease
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DOI：
10.1016/j.parkreldis.2004.01.005
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发表时间：
2004-05-01
影响因子：
4.1
通讯作者：
McGeer, EG
中科院分区：
文献类型：
--
作者：
McGeer, PL;McGeer, EG
反应性小胶质细胞和激活的补体成分的免疫组织化学证明表明，慢性炎症发生在帕金森病（PD）受影响的大脑区域。来自暴露于MPTP的人类和猴子的证据表明，这种炎症可能在最初的刺激消失后持续多年。慢性炎症会损害宿主细胞。文献中的报告表明，抗炎剂可以抑制PD动物模型中的多巴胺能细胞死亡，并且有一份流行病学报告表明，它们的使用可以显着降低人类患PD的风险。在PD的受影响区域中，补体蛋白和活化的小胶质细胞标志物的mRNA水平显著升高。这种上调似乎比在发炎的关节炎关节中发现的更大。这些数据支持慢性炎症可能在PD发病机制中起重要作用（如果是继发性的）的假设。(C)2004爱思唯尔有限公司保留所有权利。
The immunohistochemical demonstration of reactive microglia and activated complement components suggests that chronic inflammation occurs in affected brain regions in Parkinson's disease (PD). Evidence from humans and monkeys exposed to MPTP indicates this inflammation may persist many years after the initial stimulus has disappeared. Chronic inflammation can damage host cells. Reports in the literature indicate that antiinflammatory agents inhibit dopaminergic cell death in animal models of PD, and there is one epidemiological report that their use significantly diminishes the risk of PD in humans. There is a marked elevation in the mRNA levels for complement proteins and markers of activated microglia in affected regions in PD. The upregulation appears greater than that found in inflamed arthritic joints. These data support the hypothesis that chronic inflammation may play an important role, if secondary, in the pathogenesis of PD. (C) 2004 Elsevier Ltd. All rights reserved.