Connor J R, Tucker P, Johnson M, Snyder B
Department of Neuroscience and Anatomy, M.S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey 17033.
Neurosci Lett. 1993 Sep 3;159(1-2):88-90. doi: 10.1016/0304-3940(93)90805-u.
In the present study we observed a loss in excess of 1/3 of the copper transport and anti-oxidant protein ceruloplasmin in both the gray and white matter from superior temporal gyrus in Alzheimer's diseased brains compared to age-matched controls. A decrease in ceruloplasmin could be reflected in decreased cellular metabolic processes such as the electron transport system and a decrease in the ability of the brain to protect itself from oxidative damage. Both decreased metabolic activity and an increase in oxidative insults are known to be associated with the neurological events in Alzheimer's disease, but the mechanism by which these phenomena occur are unknown. These results coupled with previous reports from this laboratory on iron regulatory proteins in the brain suggests one way in which cellular dysfunction and oxidative stress occurs in AD may be through a loss of ability to maintain a balance of essential metals.
在本研究中，我们观察到，与年龄匹配的对照组相比，阿尔茨海默病患者大脑颞上回的灰质和白质中，铜转运和抗氧化蛋白铜蓝蛋白的损失超过了三分之一。铜蓝蛋白的减少可能反映在细胞代谢过程（如电子传递系统）的降低，以及大脑保护自身免受氧化损伤能力的下降。已知代谢活性降低和氧化损伤增加均与阿尔茨海默病中的神经学事件相关，但这些现象发生的机制尚不清楚。这些结果与该实验室之前关于大脑中铁调节蛋白的报告相结合，表明阿尔茨海默病中细胞功能障碍和氧化应激发生的一种方式可能是通过维持必需金属平衡的能力丧失。
