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帕金森病中抗氧化策略的神经保护作用。

Neuroprotection by anti-oxidant strategies in Parkinson's disease.

作者信息

LeWitt P A

机构信息

Wayne State University, School of Medicine, Detroit, Mich.

出版信息

Eur Neurol. 1993;33 Suppl 1:24-30. doi: 10.1159/000118534.

DOI:10.1159/000118534
PMID:8375428
Abstract

The advance of Parkinson's disease has been suspected to be an outcome of oxidative stresses related to the metabolism of dopamine. Several recent studies have tested whether deprenyl (selegiline) or alpha-tocopherol (vitamin E) might attenuate the progression of Parkinson's disease. Although preliminary results of an 800-patient controlled clinical trial (DATATOP) suggested in 1989 that neuroprotection might be achieved with deprenyl, more recent analysis has questioned this conclusion. The apparent protective effect of deprenyl is lost after 1 year of treatment, and the drug's symptomatic antiparkinsonian effects confound an understanding of actions on the underlying disease. In the DATATOP trial, no neuroprotection was achieved with alpha-tocopherol. Methods developed in the deprenyl trials and newly discovered CSF markers of Parkinson's disease may be useful tools for future investigations of neuroprotective strategies against Parkinson's disease.

摘要

帕金森病的进展被怀疑是与多巴胺代谢相关的氧化应激的结果。最近的几项研究测试了司来吉兰(丙炔苯丙胺)或α-生育酚(维生素E)是否可能减缓帕金森病的进展。尽管1989年一项纳入800名患者的对照临床试验(DATATOP)的初步结果表明,丙炔苯丙胺可能实现神经保护,但最近的分析对此结论提出了质疑。丙炔苯丙胺的明显保护作用在治疗1年后消失,而且该药物的抗帕金森病症状作用混淆了对其对潜在疾病作用的理解。在DATATOP试验中,α-生育酚未实现神经保护。丙炔苯丙胺试验中开发的方法以及新发现的帕金森病脑脊液标志物可能是未来抗帕金森病神经保护策略研究的有用工具。

相似文献

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Neuroprotection by anti-oxidant strategies in Parkinson's disease.帕金森病中抗氧化策略的神经保护作用。
Eur Neurol. 1993;33 Suppl 1:24-30. doi: 10.1159/000118534.
2
Clinical trials of neuroprotection in Parkinson's disease: long-term selegiline and alpha-tocopherol treatment.帕金森病神经保护的临床试验:长期司来吉兰和α-生育酚治疗。
J Neural Transm Suppl. 1994;43:171-81.
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The relevance of glial monoamine oxidase-B and polyamines to the action of selegiline in Parkinson's disease.胶质单胺氧化酶B和多胺与司来吉兰在帕金森病中的作用的相关性。
Mov Disord. 1993;8 Suppl 1:S8-13. doi: 10.1002/mds.870080504.
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Antioxidant mechanism and protection of nigral neurons against MPP+ toxicity by deprenyl (selegiline).抗氧化机制以及司来吉兰(丙炔苯丙胺)对黑质神经元的保护作用以抵御1-甲基-4-苯基吡啶离子(MPP+)毒性
Ann N Y Acad Sci. 1994 Nov 17;738:214-21. doi: 10.1111/j.1749-6632.1994.tb21806.x.
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Cerebrospinal fluid homovanillic acid in the DATATOP study on Parkinson's disease. Parkinson Study Group.帕金森病 DATATOP 研究中的脑脊液高香草酸。帕金森研究小组。
Arch Neurol. 1995 Mar;52(3):237-45. doi: 10.1001/archneur.1995.00540270025015.
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Pathogenesis and animal studies of Parkinson's disease.帕金森病的发病机制与动物研究
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(-)Deprenyl-medication: a strategy to modulate the age-related decline of the striatal dopaminergic system.(-)司来吉兰药物治疗:一种调节纹状体多巴胺能系统与年龄相关衰退的策略。
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A pharmacological analysis elucidating why, in contrast to (-)-deprenyl (selegiline), alpha-tocopherol was ineffective in the DATATOP study.一项药理学分析阐明了为何与(-)-司来吉兰(丙炔苯丙胺)相反,α-生育酚在DATATOP研究中无效。
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Physiology and pharmacology of dopamine D2-receptors: their implications in dopamine-substitute therapy for Parkinson's disease.多巴胺D2受体的生理学与药理学:其在帕金森病多巴胺替代疗法中的意义
Neurology. 1989 Aug;39(8):1106-8. doi: 10.1212/wnl.39.8.1106.

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Neuropsychiatr Dis Treat. 2012;8:285-94. doi: 10.2147/NDT.S25142. Epub 2012 Jul 2.