Wong-Riley M, Antuono P, Ho K C, Egan R, Hevner R, Liebl W, Huang Z, Rachel R, Jones J
Department of Cellular Biology and Anatomy, Medical College of Wisconsin, Milwaukee 53226, USA.
Vision Res. 1997 Dec;37(24):3593-608. doi: 10.1016/S0042-6989(96)00210-6.
Defects in oxidative metabolism have been implicated in Alzheimer's disease (AD). The present study evaluated the level of cytochrome oxidase (C.O.), an indicator of neuronal oxidative capacity, in various brain regions of post-mortem AD and control patients. We found a statistically significant reduction in C.O. levels in all cortical areas examined, including the primary and secondary visual cortices. In addition, all layers of the dorsal lateral geniculate nucleus and sublaminae of the primary visual cortex in AD cases examined suffered a reduction in their relative C.O. activity and protein amount. Our results suggest a generalized suppression of oxidative metabolism throughout the cortex, as well as in a major subcortical visual center in AD. Such hypometabolism may form the basis for not only deficits in higher cortical functions, but also a variety of visual dysfunctions known to occur in AD.
氧化代谢缺陷与阿尔茨海默病(AD)有关。本研究评估了细胞色素氧化酶(C.O.)的水平,它是神经元氧化能力的一个指标,在死后AD患者和对照患者的不同脑区中进行评估。我们发现在所有检查的皮质区域,包括初级和次级视觉皮质,C.O.水平有统计学上的显著降低。此外,在检查的AD病例中,背外侧膝状核的所有层以及初级视觉皮质的亚层,其相对C.O.活性和蛋白量都有所降低。我们的结果表明,在AD中,整个皮质以及一个主要的皮质下视觉中心的氧化代谢普遍受到抑制。这种代谢减退不仅可能是高级皮质功能缺陷的基础,也是已知在AD中出现的各种视觉功能障碍的基础。