Elevated oxidative stress in models of normal brain aging and Alzheimer's disease

被引:137
作者
Butterfield, DA [1 ]
Howard, B
Yatin, S
Koppal, T
Drake, J
Hensley, K
Aksenov, M
Aksenova, M
Subramaniam, R
Varadarajan, S
Harris-White, ME
Pedigo, NW
Carney, JM
机构
[1] Univ Kentucky, Ctr Membrane Sci, Dept Chem, Lexington, KY 40506 USA
[2] Univ Kentucky, Sanders Brown Ctr Aging, Lexington, KY 40506 USA
[3] Univ Kentucky, Dept Pharmacol, Lexington, KY 40506 USA
[4] Centaur Pharmaceut, Sunnyvale, CA 94086 USA
关键词
protein oxidation; free radicals; lipid peroxidation; hydroxynonenal; beta-amyloid; aging; Alzheimer's disease;
D O I
10.1016/S0024-3205(99)00442-7
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Age-associated neurodegenerative disorders are becoming more prevalent as the mean age of the population increases in the United States over the next few decades. Both normal brain aging and Alzheimer's disease (AD) are associated with oxidative stress. Our laboratory has used a wide variety of physical and biochemical methods to investigate free radical oxidative stress in several models of aging and AD. beta-amyloid (A beta), the peptide that constitutes the central core of senile plaques in AD brain, is associated with free radical oxidative stress and is toxic to neurons. This review summarizes some of our studies in aging and A beta-associated free radical oxidative stress and on the modulating effects of free radical scavengers on neocortical synaptosomal membrane damage found in aging and A beta-treated systems.
引用
收藏
页码:1883 / 1892
页数:10
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