| Literature DB >> 9063589 |
G Münch1, J Thome, P Foley, R Schinzel, P Riederer.
Abstract
Accumulation of advanced glycation endproducts (AGE) in the brain is a feature of 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 (beta-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 may be a promising neuroprotective strategy.Entities:
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Year: 1997 PMID: 9063589 DOI: 10.1016/s0165-0173(96)00016-1
Source DB: PubMed Journal: Brain Res Brain Res Rev