PURPOSE Corneal complications are often associated with diabetes mellitus and can be vision threatening. Corneas in diabetic patients are exposed to increased glucose concentration despite cornea's avascular property, and this condition may contribute to the accumulation of advanced glycation end products (AGEs). The focus of this study was to examine the role of AGEs in the pathogenesis of dia...

Chronic hyperglycemia and oxidative stress in diabetes results in the formation and accumulation advanced glycation end products (AGEs). AGEs have a wide range of chemical, cellular, and tissue effects that contribute to the development of microvascular complications. In particular, AGEs appear to have a key role in the diabetic nephropathy. Their importance as downstream mediators of tissue in...

The reaction between reducing sugars and protein free amines, known as the Maillar reaction results in the formation of advanced glycation endproducts (AGEs). AGE modification changes the structure of proteins to amyloid cross-beta structure. These protein structures can activate receptors known as RAGE on glial cells (microglia and astrocytes), and induce the expression of inducible nitric oxi...

advanced glycation end-products (ages) are formed by non-enzymatic reaction between reducing sugar and protein. ages play important roles in pathogenesis of diabetic, aging complications, endothelial dysfunction and neurological diseases such as the alzheimer’s disease. therefore compounds that prevent the glycation reaction are purported to have therapeutic effect on patients with diabetes and...

Glycation is a protein modification, which results in a change in a protein structure. Glycation is believed to be the etiology of various age-related diseases such as diabetes mellitus and Alz-heimer’s disease (AD). Activation of microglia and resident macrophages in the brain by glycated proteins with subsequent oxidative stress and cytokine release may be an important factor in the progressi...

It is becoming abundantly clear that the insight into the pathological process of Alzheimer’s disease (AD) provided through autosomal dominant variants of the condition is only a partial one. The formation and aggregation of Aβ and the phosphorylation and aggregation of tau are clearly part of the core pathogenesis. However, although these may be necessary processes, and indeed in familial form...