Glycoxidative stress creates a vicious cycle of neurodegeneration in Alzheimer's disease--a target for neuroprotective treatment strategies?
Accumulation of Advanced Glycation Endproducts (AGEs) 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), glial activation, 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, anti-inflammatory drugs and AGE-inhibitors may be a promising neuroprotective strategy.
Münch
G
G
Neuroimmunological Cell Biology, Interdisciplinary Center of Clinical Research (IZKF), Leipzig, Federal Republic of Germany. mueg@medizin.uni-leipzig.de
Deuther-Conrad
W
W
Gasic-Milenkovic
J
J
D000368:Aged; D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism*; D015195:Drug Design; D017127:Glycation End Products, Advanced / Q000378:metabolism*; D006801:Humans; D009410:Nerve Degeneration / Q000188:drug therapy / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000627:therapeutic use*
D017127:Glycation End Products, Advanced; D018696:Neuroprotective Agents