散发性神经退行性疾病中线粒体 DNA 相关的线粒体功能障碍的作用和治疗。
Role and treatment of mitochondrial DNA-related mitochondrial dysfunction in sporadic neurodegenerative diseases.
机构信息
Department of Neurology, University of Kansas School of Medicine, Kansas City, 66160, USA.
出版信息
Curr Pharm Des. 2011;17(31):3356-73. doi: 10.2174/138161211798072535.
Abstract
Several sporadic neurodegenerative diseases display phenomena that directly or indirectly relate to mitochondrial function. Data suggesting altered mitochondrial function in these diseases could arise from mitochondrial DNA (mtDNA) are reviewed. Approaches for manipulating mitochondrial function and minimizing the downstream consequences of mitochondrial dysfunction are discussed.
摘要
几种散发性神经退行性疾病表现出与线粒体功能直接或间接相关的现象。本文回顾了提示这些疾病中线粒体功能改变的数据，这些数据可能源于线粒体 DNA（mtDNA）。讨论了操纵线粒体功能和最小化线粒体功能障碍下游后果的方法。
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本文引用的文献
1
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Pharmaceuticals (Basel). 2009 Dec 3;2(3):150-167. doi: 10.3390/ph2030150.
2
Progressive regional atrophy in normal adults with a maternal history of Alzheimer disease.有阿尔茨海默病母系病史的正常成年人进行性区域性萎缩。
Neurology. 2011 Mar 1;76(9):822-9. doi: 10.1212/WNL.0b013e31820e7b74.
3
Does mitochondrial DNA play a role in Parkinson's disease? A review of cybrid and other supportive evidence.线粒体 DNA 在帕金森病中起作用吗？对细胞融合和其他支持性证据的综述。
Antioxid Redox Signal. 2012 May 1;16(9):950-64. doi: 10.1089/ars.2011.3948. Epub 2011 May 25.
4
Structural brain changes in normal individuals with a maternal history of Alzheimer's.有阿尔茨海默病家族史的正常个体的大脑结构变化。
Neurobiol Aging. 2011 Dec;32(12):2325.e17-26. doi: 10.1016/j.neurobiolaging.2011.01.001. Epub 2011 Feb 12.
5
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