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阿尔茨海默病和帕金森病中的线粒体功能障碍与氧化损伤以及辅酶Q10作为一种潜在治疗方法

Mitochondrial dysfunction and oxidative damage in Alzheimer's and Parkinson's diseases and coenzyme Q10 as a potential treatment.

作者信息

Beal M Flint

机构信息

Department of Neurology and Neuroscience, New York Presbyterian Hospital-Weill Medical College of Cornell University, 525 East 68th Street, New York, New York 10021, USA.

出版信息

J Bioenerg Biomembr. 2004 Aug;36(4):381-6. doi: 10.1023/B:JOBB.0000041772.74810.92.

DOI:10.1023/B:JOBB.0000041772.74810.92
PMID:15377876
Abstract

There is substantial evidence that mitochondrial dysfunction and oxidative damage may play a key role in the pathogenesis of neurodegenerative disease. Evidence supporting this in both Alzheimer's and Parkinson's diseases is continuing to accumulate. This review discusses the increasing evidence for a role of both mitochondrial dysfunction and oxidative damage in contributing to beta-amyloid deposition in Alzheimer's disease. I also discuss the increasing evidence that Parkinson's disease is associated with abnormalities in the electron transport gene as well as oxidative damage. Lastly, I reviewed the potential efficacy of coenzyme Q as well as a number of other antioxidants in the treatment of both Parkinson's and Alzheimer's diseases.

摘要

有大量证据表明，线粒体功能障碍和氧化损伤可能在神经退行性疾病的发病机制中起关键作用。支持这一观点的证据在阿尔茨海默病和帕金森病中都在不断积累。本综述讨论了越来越多的证据表明，线粒体功能障碍和氧化损伤在阿尔茨海默病中β-淀粉样蛋白沉积中所起的作用。我还讨论了越来越多的证据表明，帕金森病与电子传递基因异常以及氧化损伤有关。最后，我回顾了辅酶Q以及其他一些抗氧化剂在治疗帕金森病和阿尔茨海默病方面的潜在疗效。

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本文引用的文献

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