Parker W D, Filley C M, Parks J K
Department of Neurology, School of Medicine, University of Colorado Health Sciences Center, Denver 80262.
Neurology. 1990 Aug;40(8):1302-3. doi: 10.1212/wnl.40.8.1302.
We assayed cytochrome oxidase and other electron transport chain activities in platelet mitochondria isolated from patients with Alzheimer's disease (AD). Five of 6 patients had striking reductions of platelet cytochrome oxidase activity (patient mean, 83.72 +/- 82.99 nmol/min/mg; control mean, 167.14 +/- 36.21 nmol/min/mg; n = 8). Other electron transport chain catalytic activities were not significantly different than control values. AD may be a systemic illness, a primary defect in cytochrome oxidase may be pathogenically important in its production, and the mitochondrial genes encoding cytochrome oxidase subunits may be important in producing the defect.
我们检测了从阿尔茨海默病（AD）患者分离出的血小板线粒体中的细胞色素氧化酶及其他电子传递链活性。6例患者中有5例血小板细胞色素氧化酶活性显著降低（患者平均值为83.72±82.99纳摩尔/分钟/毫克；对照组平均值为167.14±36.21纳摩尔/分钟/毫克；n = 8）。其他电子传递链催化活性与对照组值无显著差异。AD可能是一种全身性疾病，细胞色素氧化酶的原发性缺陷在其发病机制中可能具有重要意义，并且编码细胞色素氧化酶亚基的线粒体基因在产生该缺陷方面可能很重要。
