It is apparent that advanced glycosylation end products (AGEs) contribute to nerve damage either by direct action on neurons and myelin or by enhancing oxidative stress under hyperglycemic conditions. Thus, there is a great deal of interest in agents that either prevent the formation of AGEs or agents that reverse the nonenzymatic glycation of proteins.
Animal studies using aminoguanidine, an inhibitor of the formation of AGEs, showed improvement in nerve conduction velocity in rats with STZ-induced diabetic neuropathy. However, controlled clinical trials to determine its efficacy in humans have been discontinued because of toxicity (19,20). However, there are compounds related to aminoguanidine that reduced AGE formation and hold promise for this approach, although these have not been systematically studied in humans (21-24).
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