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环氧化酶-2与帕金森病中的神经退行性变

COX-2 and neurodegeneration in Parkinson's disease.

作者信息

Teismann P, Vila M, Choi D-K, Tieu K, Wu D C, Jackson-Lewis V, Przedborski S

机构信息

Neuroscience Research Laboratories of the Movement Disorder Division, Department of Neurology, Columbia University, New York, New York 10032, USA.

出版信息

Ann N Y Acad Sci. 2003 Jun;991:272-7. doi: 10.1111/j.1749-6632.2003.tb07482.x.

Abstract

Parkinson's disease (PD) is a common neurodegenerative disorder characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Recent observations link cyclooxygenase type-2 (COX-2) to the progression of the disease. Consistent with this notion, studies with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) show that inhibition and ablation of COX-2 markedly reduce the deleterious effects of this toxin on the nigrostriatal pathway. The similarity between this experimental model and PD strongly supports the possibility that COX-2 expression is also pathogenic in PD.

摘要

帕金森病(PD)是一种常见的神经退行性疾病,其特征是黑质致密部多巴胺能神经元进行性丧失。最近的观察结果将2型环氧化酶(COX-2)与该疾病的进展联系起来。与此观点一致,使用多巴胺能神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)的研究表明,COX-2的抑制和缺失显著降低了这种毒素对黑质纹状体通路的有害影响。这个实验模型与帕金森病之间的相似性有力地支持了COX-2表达在帕金森病中也具有致病性的可能性。

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