Mutisya E M, Bowling A C, Beal M F
Neurochemistry Laboratory, Massachusetts General Hospital, Boston 02114.
J Neurochem. 1994 Dec;63(6):2179-84. doi: 10.1046/j.1471-4159.1994.63062179.x.
A defect in energy metabolism may play a role in the pathogenesis of neurodegenerative diseases, such as Alzheimer's disease. In the present study, we examined the activities of the enzymes that catalyze oxidative phosphorylation in frontal, temporal, parietal, and occipital cortex from Alzheimer's disease patients and age-matched controls. Complex I and complex II-III activities showed a small decrease in occipital cortex, but were unaffected in the other cortical areas. The most consistent change was a significant decrease of cytochrome oxidase (complex IV) activity of 25-30% in the four cortical regions examined. These results provide further evidence of a cytochrome oxidase defect in Alzheimer's disease postmortem brain tissue. A deficiency in this key energy-metabolizing enzyme could lead to a reduction in energy stores and thereby contribute to the neurodegenerative process.
能量代谢缺陷可能在神经退行性疾病(如阿尔茨海默病)的发病机制中起作用。在本研究中,我们检测了阿尔茨海默病患者及年龄匹配的对照者额叶、颞叶、顶叶和枕叶皮质中催化氧化磷酸化的酶的活性。复合体I和复合体II - III的活性在枕叶皮质略有下降,但在其他皮质区域未受影响。最一致的变化是在所检测的四个皮质区域中,细胞色素氧化酶(复合体IV)的活性显著降低了25% - 30%。这些结果为阿尔茨海默病死后脑组织中存在细胞色素氧化酶缺陷提供了进一步证据。这种关键的能量代谢酶的缺乏可能导致能量储备减少,从而促进神经退行性变过程。