Given the role played by advanced glycation end-products (AGEs) in aging, scientists continue to search for ways to destroy or limit the accumulation of these compounds. Regulation generally forces such studies to relate to the treatment of age-related diabetes - intervention in aging is not recognized as a legitimate field of research by the FDA, so therapies will not be approved for use, and thus funding cannot be found for development. "We investigated the effects of various concentrations of a compound, LR-90, on the progression of renal disease and its effects on AGE and receptor for AGE (RAGE) protein expression on the kidneys of [diabetic rats] ... LR-90 treatment [reduced] kidney AGE/ALE accumulation and RAGE protein expression ... In vitro, LR-90 exhibited general antioxidant properties ... The compound also prevents AGE-protein cross-linking reactions. These findings demonstrate the bioefficacy of LR-90 in treating [diabetic animals] by inhibiting AGE accumulation, RAGE protein expression, and protein oxidation in the diabetic kidney. Additionally, our study suggests that LR-90 may be useful also to delay the onset and progression of diabetic atherosclerosis." All of which would be beneficial as applied to normal aging - assuming that this compound is useful in people. Most prospective AGE-breakers coming from animal studies fail to do much good in humans, as the mix of AGE compounds is quite different.

Link: http://www.ncbi.nlm.nih.gov/pubmed/17709884