Advanced gly cation end-products

Wang, X., Desai, K., Clausen, J.T., and Wu, L. 2004. Increased methylglyoxal and advanced gly-cation end products in kidney from spontaneously hypertensive rats. Kidney Int 66 2315-2321. 

Evidence of selective oxidative damage, resulting from redox imbalance, involving neurons tied to AD is accumulating. The advanced gly-cation end products, nitration, lipid peroxidation adduction products, carbonyl-modified neurofilament protein, and free carbonyls belong to the list (200). The question remains whether the oxidative damage is caused by A)3, known to possess oxidative and hydrolytic properties (286, 287), or by other factors, whereas Aj3 is released as an antioxidant in response to oxidative stress (200). As in other groups of potential AD therapeutics there is a noticeable difference between their behavior in vitro and in vivo. A number of potential antioxidants are or have been in clinical trials... 

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