Tranchant C, Weess C, Warter J M
Service des Maladies du Système Nerveux et du Muscle, CHU, Strasbourg.
Rev Neurol (Paris). 1995 Mar;151(3):157-60.
Work on the molecular mechanisms of MPTP neurotoxicity have inspired search into the function of mitochondria in idiopathic Parkinson's disease. All the studies show a decrease of 30 to 40% in the activity of the respiratory complex I in the mitochondria of the nigra substantia. This decreased activity is not found in other degenerative Parkinsonisms treated with L-Dopa and cannot be explained simply by age. It is not found in other tissues including muscles and platelets. The causal mechanism of this mitochondrial dysfunction is unknown but it is not related to a mutation in mitochondrial DNA.
对MPTP神经毒性分子机制的研究激发了人们对特发性帕金森病中线粒体功能的探索。所有研究均表明，黑质线粒体中呼吸复合体I的活性降低了30%至40%。在用左旋多巴治疗的其他退行性帕金森综合征中未发现这种活性降低，也不能简单地用年龄来解释。在包括肌肉和血小板在内的其他组织中也未发现这种情况。这种线粒体功能障碍的因果机制尚不清楚，但与线粒体DNA突变无关。
