Hunot Stephane, Hirsch E C
INSERM U289, Hôpital de la Salpêtrière, Paris, France.
Ann Neurol. 2003;53 Suppl 3:S49-58; discussion S58-60. doi: 10.1002/ana.10481.
Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory-associated factors such as cyclooxygenase-2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD.
帕金森病(PD)是一种运动障碍性疾病,其特征是中脑多巴胺能神经元进行性退化。迄今为止,其病因尚不清楚,神经细胞死亡机制也不确定。除了多巴胺能神经元大量丧失外,帕金森病患者的大脑还表现出明显的胶质细胞反应以及神经炎症反应迹象,表现为细胞因子水平升高和炎症相关因子如环氧合酶-2和诱导型一氧化氮合酶上调。越来越多的证据还表明,这些神经炎症过程在该疾病的实验模型中可能具有有害作用。我们提出,在帕金森病中,神经炎症在导致神经细胞死亡的一系列事件中起作用,从而推动神经退行性过程。在这篇综述中,我们总结并讨论了帕金森病神经炎症方面的最新研究结果。