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 (β-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.
CITATION STYLE
Münch, G., Deuther-Conrad, W., & Gasic-Milenkovic, J. (2002). Glycoxidative stress creates a vicious cycle of neurodegeneration in Alzheimer’s disease - A target for neuroprotective treatment strategies? In Journal of Neural Transmission, Supplement (pp. 303–307). Springer Wien. https://doi.org/10.1007/978-3-7091-6139-5_28
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