Advanced glycation endproducts in ageing and Alzheimer's disease

被引：247

作者：

Munch, G ^{[1
]}

Thome, J ^{[1
]}

Foley, P ^{[1
]}

SChinzel, R ^{[1
]}

Riederer, P ^{[1
]}

机构：

[1] DEPT PSYCHIAT,D-97080 WURZBURG,GERMANY

来源：

BRAIN RESEARCH REVIEWS | 1997年 / 23卷 / 1-2期

关键词：

advanced glycation end product; neurodegeneration; oxidative stress; Alzheimer's disease; plaque; tangle; neurotoxicity;

D O I：

10.1016/S0165-0173(96)00016-1

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Accumulation of advanced glycation endproducts (AGE) in the brain is a feature or ageing and degeneration, especially in Alzheimer's disease (AD). Increased AGE levels explain many of the neuropathological and biochemical features of AD such as extensive protein crosslinking (alpha-amyloid and MAP-tau), oxidative stress and neuronal cell death. Oxidative stress and AGEs initiate a positive feedback loop, where normal age-related changes develop into a pathophysiological cascade. Combined intervention using antioxidants, metal chelators, anti-inflammatory drugs and AGE-inhibitors map be a promising neuroprotective strategy.

引用

页码：134 / 143

页数：10

共 78 条

[1] MACROPHAGE SCAVENGER RECEPTOR MEDIATES THE ENDOCYTIC UPTAKE AND DEGRADATION OF ADVANCED GLYCATION END-PRODUCTS OF THE MAILLARD REACTION [J].