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 (alp
ha-amyloid and MAP-tau), oxidative stress and neuronal cell death. Oxi
dative stress and AGEs initiate a positive feedback loop, where normal
age-related changes develop into a pathophysiological cascade. Combin
ed intervention using antioxidants, metal chelators, anti-inflammatory
drugs and AGE-inhibitors map be a promising neuroprotective strategy.