Parker W D, Parks J, Filley C M, Kleinschmidt-DeMasters B K
Department of Neurology, University of Colorado School of Medicine, Denver.
Neurology. 1994 Jun;44(6):1090-6. doi: 10.1212/wnl.44.6.1090.
Previous work suggested a deficiency in the terminal complex of the mitochondrial electron transport chain, cytochrome c oxidase (COX), in platelet mitochondria of Alzheimer's disease (AD) patients. The present study extends this observation to AD brain mitochondria through assay of electron transport chain activities in mitochondria isolated from autopsied brain samples from AD patients (n = 9) and from controls with and without known neurologic disease (n = 8). AD brain mitochondria demonstrated a generalized depression of activity of all electron transport chain complexes. This depression was most marked in COX activity (p < 0.001). Concentrations of cytochromes b, c1, and aa3 were similar in AD and controls. The electron transport chain is defective in AD brain, and the defect centers about COX.
先前的研究表明，阿尔茨海默病（AD）患者血小板线粒体中的线粒体电子传递链终末复合物——细胞色素c氧化酶（COX）存在缺陷。本研究通过检测从AD患者（n = 9）以及有或无已知神经疾病的对照者（n = 8）的尸检脑样本中分离出的线粒体中的电子传递链活性，将这一观察结果扩展至AD脑线粒体。AD脑线粒体显示出所有电子传递链复合物活性普遍降低。这种降低在COX活性中最为明显（p < 0.001）。AD组和对照组中细胞色素b、c1和aa3的浓度相似。AD脑的电子传递链存在缺陷，且该缺陷集中在COX。
