The formation of advanced glycation end products (AGEs) is a key pathophysiological event with links to a range of important human diseases. It is now clear that AGEs may act as mediators, not only of diabetic complications1 ,2 but also of widespread age related pathology such as Alzheimer's disease,3 decreased skin elasticity,4 ,5 male erectile dysfunction,6 ,7 pulmonary fibrosis,8 and atherosclerosis.9 ,10 Since many cells and tissues of the eye are profoundly influenced by both diabetes and ageing, it is fitting that advanced glycation is now receiving considerable attention as a possible modulator in important visual disorders. An increasing number of reports confirm widespread AGE accumulation at sites of known ocular pathology and demonstrate how these products mediate crosslinking of long lived molecules in the eye. Such studies also underscore the putative pathophysiological role of advanced glycation in ocular cell dysfunction in vitro and in vivo.

This article reviews some of the important effects that advanced glycation has on ocular tissues and the role that AGEs, and their specific receptors, have in the initiation and progression of sight threatening disorders such as diabetic retinopathy, glaucoma, cataract formation, and age related macular degeneration (AMD). This review also considers pharmacological strategies to prevent or neutralise the effects of AGEs and the recent development of potential therapies for AGE induced disease processes.