Smith M A, Perry G
Institute of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
J Neurol Sci. 1995 Dec;134 Suppl:92-4. doi: 10.1016/0022-510x(95)00213-l.
We present evidence to support the premise that many of the pathological correlates of Alzheimer's disease are precipitated by free radical- and oxidative stress-induced mechanisms. We propose that amyloid-beta deposition in senile plaques, intracellular accumulation of protein in neurofibrillary tangles, and the degeneration of specific neuronal populations can be attributed to specific oxidative stress-type mechanisms. Free radicals in disease pathogenesis, generated in part as a result of Fenton-type reactions, suggest that lowering the level of available iron, intervention with antioxidants, or the administration of free radical scavengers could provide a therapeutic inroad in the fight against Alzheimer's disease.
我们提供证据支持这样一个前提，即阿尔茨海默病的许多病理相关因素是由自由基和氧化应激诱导的机制所引发的。我们提出，老年斑中的β淀粉样蛋白沉积、神经原纤维缠结中的蛋白质细胞内积累以及特定神经元群体的退化可归因于特定的氧化应激型机制。疾病发病机制中的自由基部分是由芬顿型反应产生的，这表明降低可用铁的水平、使用抗氧化剂进行干预或给予自由基清除剂可能为对抗阿尔茨海默病提供一条治疗途径。
