期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 5, 期 1, 页码 25-30出版社
IOS PRESS
DOI: 10.3233/JAD-2003-5104
关键词
Glycation; Alzheimer's disease; lipid peroxidation; antioxidants; RAGE; alpha-lipoic acid; hydroxynonenal
资金
- Alzheimer Forschungs-Initiative e.V. (AFI)
- Hirnliga
- SmithKlineBeecham-Stiftung
- Bun-desministerium fur Bildung, Forschung und Technologie (BMB+F)
- Interdisziplinares Zentrum fur Klinische Forschung (IZKF) at the University of Leipzig [01KS9504]
- EU [QLK6-CT-1999-02112]
- Alexander von Humboldt Stiftung
Advanced glycation endproducts (AGEs), sugar-derived protein modifications and lipid peroxidation products are prominent features of Alzheimer's disease. AGEs accumulate on beta-amyloid plaques during the course of the disease and can exert chronic oxidative stress via receptor-mediated mechanisms. Lipid peroxidation products such as hydroxynonenal, further markers of oxidative stress, are also increased in Alzheimer's diesease. In this study we present evidence for a direct biochemical link between AGEs and lipid peroxidation. Our results show that AGEs induce lipid peroxidation in a neuronal cell line in a dose-dependant manner, and that blocking the specific AGE-receptor RAGE, as well as using different antioxidants (alpha-lipoic acid, N-acetylcysteine, 17 beta-estradiol or aminoguanidine) can reduce the AGE-mediated formation of lipid peroxidation products. Thus, both RAGE antagonists and scavengers of oxygen free radicals could be useful in protecting brain tissue from lipid peroxidation and its pathophysilogical consequences that occur in Alzheimer's disease.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据