Moreira Paula I, Zhu Xiongwei, Liu Quan, Honda Kazuhiro, Siedlak Sandra L, Harris Peggy L, Smith Mark A, Perry George
Institute of Pathology, Case Western Reserve University, 2085 Adelbert Road, Cleveland, OH 44100, USA.
Biol Res. 2006;39(1):7-13. doi: 10.4067/s0716-97602006000100002.
Oxidative stress occurs early in the progression of Alzheimer disease, significantly before the development of the pathologic hallmarks, neurofibrillary tangles and senile plaques. In the first stage of development of the disease, amyloid-beta deposition and hyperphosphorylated tau function as compensatory responses and downstream adaptations to ensure that neuronal cells do not succumb to oxidative damage. These findings suggest that Alzheimer disease is associated with a novel balance in oxidant homeostasis.
氧化应激在阿尔茨海默病进展的早期就会出现，远早于病理特征——神经原纤维缠结和老年斑的形成。在疾病发展的第一阶段，β-淀粉样蛋白沉积和过度磷酸化的tau蛋白起到代偿反应和下游适应性作用，以确保神经元细胞不会因氧化损伤而死亡。这些发现表明，阿尔茨海默病与氧化还原稳态中的一种新平衡有关。
