McGeer Edith G, McGeer Patrick L
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, British Columbia, Canada.
CNS Drugs. 2007;21(10):789-97. doi: 10.2165/00023210-200721100-00001.
There is ample and increasing evidence, from studies of human pathology, animal models and tissue culture, that chronic inflammation occurs in the basal ganglia in patients with Parkinson's disease. In such inflammatory states, activated glia can produce large quantities of free radicals and other neurotoxic materials. Dopaminergic neurons appear to be particularly vulnerable to these neurotoxins. The anti-inflammatory drugs that are presently in wide use act on peripheral players in the inflammatory process. Many experiments are under way to find agents that inhibit more potent contributors, such as the activated microglia or terminal complement proteins. Whether such drugs will slow the process of Parkinson's disease or reduce the high risk of dementia in such patients remains to be determined in future work.
来自人体病理学、动物模型和组织培养研究的证据充分且不断增加,表明帕金森病患者的基底神经节会发生慢性炎症。在这种炎症状态下,活化的神经胶质细胞可产生大量自由基和其他神经毒性物质。多巴胺能神经元似乎对这些神经毒素特别敏感。目前广泛使用的抗炎药物作用于炎症过程中的外周参与者。目前正在进行许多实验,以寻找能够抑制更有效促炎因素的药物,如活化的小胶质细胞或终末补体蛋白。这类药物是否会减缓帕金森病的进程或降低此类患者患痴呆症的高风险,仍有待未来的研究来确定。