帕金森病和衰老过程中纹状体中线粒体DNA缺失增加。
Increase of deleted mitochondrial DNA in the striatum in Parkinson's disease and senescence.
作者信息
Ikebe S, Tanaka M, Ohno K, Sato W, Hattori K, Kondo T, Mizuno Y, Ozawa T
机构信息
Department of Biomedical Chemistry, Faculty of Medicine, University of Nagoya, Japan.
出版信息
Biochem Biophys Res Commun. 1990 Aug 16;170(3):1044-8. doi: 10.1016/0006-291x(90)90497-b.
A mutant mitochondrial DNA (mtDNA) with a 4,977-bp deletion was detected in the parkinsonian brain by using the polymerase chain reaction. Although the deleted mtDNA was detectable even in the brain of aged controls, the proportion of deleted mtDNA to normal mtDNA in the striatum was higher in the parkinsonian patients than in the controls. In both the parkinsonian patients and the aged controls, the proportion was higher in the striatum than in the cerebral cortex. These results indicate that age-related accumulation of deleted mtDNA is accelerated in the parkinsonian striatum and suggest that the deletion contributes to pathophysiological processes underlying Parkinson's disease.
通过聚合酶链反应在帕金森病患者的大脑中检测到一种有4977个碱基对缺失的突变线粒体DNA（mtDNA）。尽管在老年对照者的大脑中也能检测到缺失的mtDNA，但帕金森病患者纹状体中缺失的mtDNA与正常mtDNA的比例高于对照者。在帕金森病患者和老年对照者中，纹状体中的这一比例均高于大脑皮层。这些结果表明，帕金森病患者纹状体中与年龄相关的缺失mtDNA积累加速，提示这种缺失参与了帕金森病的病理生理过程。
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