Abstract
Age-related macular degeneration (AMD), the leading cause of blindness in the elderly, is characterized by progressive damage to supportive layers and photoreceptor cell loss. No current therapy halts vision loss. Numerous genetic and/or environmental factors likely contribute to the initiating events leading to AMD. Progressive events from cellular dysfunction and tissue destruction result in the histopathological features of AMD including drusen formation, basal laminar deposits, accumulation of lipofuscin in the retinal pigmented epithelium (RPE), thickening of Bruch's membrane, choriovasculature and RPE cell loss, and photoreceptor cell death. Studies on the biochemical and physiological perturbations seen in the RPE, Bruch's membrane and the choroid correlate well with AMD, however, progressive events leading to these characteristic features are not well understood. Resolving these issues is essential for successful therapeutic intervention of AMD. We propose that receptor-mediated cellular activation by advanced glycation end (AGE) products, a major contributor to progressive tissue damage in other aging disorders, may also contribute significantly to progressive damage in AMD. In this paper, we review and compare pathological features of AMD to AGE/RAGE- mediated progressive events incurred in other aging disorders.
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