Last update:
10-Sep-2004

Advanced glycated end products (AGEs) arise from the non-enzymatic glycosylation of proteins, lipids, and nucleic acids by glucose. The AGE modified macromolecules have the ability to crosslink and to act as traps of plasma proteins, interfering in this way with tissue function. The cells which have receptors for AGEs are monocytes/macrophages, endothelial cells, T-lymphocytes, fibroblasts, mesangial cells and smooth muscle cells. Under normal conditions the interaction of AGEs with their receptors initiates a cascade of cytokines and growth factors involved in protein degradation and tissue repair. In pathological conditions such as diabetes mellitus because of hyperglycemia, this cascade operates in an accelerated mode and leads to tissue hyperplasia. AGEs have been associated with the etiopathogenesis in diabetes mellitus of atherosclerosis, nephropathy, neuropathy, retinopathy, diabetic hand syndrome, and possibly embryopathy. They have also been implicated in Alzheimer's and Parkinson's diseases, and in the process of aging. Designing AGE inhibitors is the main therapeutic target nowadays for the management of AGE associated conditions. Aminoguanidin is a compound which inhibits the conversion of the early glycation Amadori products to AGEs and is currently under phase III clinical trials for diabetic nephropathy. Healthy diet, avoidance of smoking and consumption of anti-oxidants such as vitamins C and E can complement therapy. Further research on AGEs will aid in the understanding and treatment of the conditions associated with their production.

Key words: Advanced glycated end products, AGE inhibitors, AGE receptors, Alzheimer, Diabetes mellitus.