Advanced glycation endproducts

Advanced glycation end products (AGEs) are proteins or lipids that become glycated as a result of exposure to sugars. They can be a factor in aging and in the development or worsening of many degenerative diseases, such as diabetes, atherosclerosis, chronic kidney disease, and Alzheimer's disease.

AGEs affect nearly every type of cell and molecule in the body and are thought to be one factor in aging and some age-related chronic diseases. They are also believed to play a causative role in the vascular complications of diabetes mellitus.

Under certain pathologic conditions, such as oxidative stress due to hyperglycemia in patients with diabetes, and hyperlipidemia, AGE formation can be increased beyond normal levels. AGEs are now known to play a role as proinflammatory mediators in gestational diabetes as well.

The animal and human evidence is that significant amounts of dietary advanced glycation end-products (dAGEs) are absorbed, and that dAGEs contribute to the body's burden of AGE, and are associated with diseases such as atherosclerosis and kidney disease.

In the context of cardiovascular disease, AGEs can induce crosslinking of collagen which can cause vascular stiffening and entrapment of low-density lipoprotein particles (LDL) in the artery walls. AGEs can also cause glycation of LDL which can promote its oxidation. Oxidized LDL is one of the major factors in the development of atherosclerosis. Finally, AGEs can bind to RAGE (receptor for advanced glycation end products) and cause oxidative stress as well as activation of inflammatory pathways in vascular endothelial cells.

The formation and accumulation of advanced glycation endproducts (AGEs) has been implicated in the progression of age-related diseases. AGEs have been implicated in Alzheimer's Disease, cardiovascular disease, and stroke. The mechanism by which AGEs induce damage is through a process called cross-linking that causes intracellular damage and apoptosis. They form photosensitizers in the crystalline lens, which has implications for cataract development. Reduced muscle function is also associated with AGEs.

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