The Effect of Advanced Glycation End Product Inhibition on the Development of Diabetic Encephalopathy in Rats

Abstract

Advanced glycation end product (AGE) endogenous proliferation has been identified as a result of long term hyperglycemia associated with diabetes metillus. These products have been linked to various problems of aging and diabetes. This study used diabetic and non-diabetic rats. Each group received either the placebo, or the AGE inhibitor, aminoguanidine. The animals were then cognitively evaluated after eight weeks. I hypothesized that, diabetic rats receiving aminoguanidine would show reduced cognitive decline as compared with diabetic rats not receiving aminoguanidine. My observations support my hypothesis.