Free radical damage, iron, and Alzheimer's disease

被引：107

作者：

Smith, MA ^{[1
]}

Perry, G ^{[1
]}

机构：

[1] CASE WESTERN RESERVE UNIV,INST PATHOL,CLEVELAND,OH 44106

来源：

JOURNAL OF THE NEUROLOGICAL SCIENCES | 1995年 / 134卷

关键词：

Alzheimer's disease; free radicals; glycation; iron; neurofibrillary pathology; oxidative stress; senile plaques;

D O I：

10.1016/0022-510X(95)00213-L

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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.

引用

页码：92 / 94

页数：3

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