Neuroinflammatory processes in Parkinson's disease
Neuroinflammatory processes in Parkinson's disease
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DOI：
10.1016/j.parkreldis.2004.10.013
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发表时间：
2005-06-01
影响因子：
4.1
通讯作者：
Hartmann, A
中科院分区：
文献类型：
--
作者：
Hirsch, EC;Hunot, S;Hartmann, A
在帕金森氏病（PD）中，尸检显示黑质（SN）中多巴胺能（DA）神经元的丢失与大量星形胶质细胞增生和活化的小胶质细胞的存在相关。类似地，还报道了在由1-甲基-4-苯基-1，2，3，6-四氢吡啶（MPTP）、鱼藤酮、番荔枝碱和脂多糖（LPS）诱导的PD动物模型中，小胶质细胞活化与DA神经元的损失相关。最近的证据表明，即使神经元变性的最初原因已经消失，这种疾病也可能进展，这增加了神经胶质细胞释放的有毒物质可能参与神经元变性传播的可能性。因此，抑制神经胶质反应和炎症过程可能是减少PD神经元变性的治疗靶点。(C)2005爱思唯尔有限公司保留所有权利。
In Parkinson's disease (PD), post-mortem examination reveals a loss of dopaminergic (DA) neurons in the substantia nigra (SN) associated with a massive astrogliosis and the presence of activated microglial cells. Similarly, microglial activation has also been reported to be associated with the loss of DA neurons in animal models of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, annonacine and lipopolysaccharide (LPS). Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, raising the possibility that toxic substances released by glial cells could be involved in the propagation of neuronal degeneration. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in PD. (C) 2005 Elsevier Ltd. All rights reserved.