Programm                 "Degeneration und Regeneration– Grundlagen, Diagnostik und Therapie"


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Abstract
Abstract

Impact of RPE-dysfunction on AMD Pathogenesis

Schütt F.
Department of Ophthalmology, University of Heidelberg

Age-related macular degeneration (AMD) is now the most common cause of registerable blindness in the Western nations beyond 50 years of age. The pathogenesis of AMD is still incompletely understood. Several lines of evidence suggest that the retinal pigment epithelium (RPE) plays a key role in the pathogenesis of AMD. It is evident that the RPE cell layer is involved in all clinical ARMD phenotypes. The RPE has numerous functions that are a prerequisite for normal photoreceptor function including permanent phagocytosis, degradation and clearance of shed distal outer photoreceptor segments. Every derangement in the balance of phagocytotic and degradative processes may result in incomplete catabolism and accumulation of biomolecules as lipofuscin (LF). LF accumulates in the RPE throughout life and with various retinal diseases eventually occupying up to 19% of cytoplasmic volume by 80 years of age. Within areas of increased LF-mediated fundus autofluorescence, new atrophic areas develop, and existing patches of atrophy enlarge. Corresponding photoreceptor density and retinal sensitivity are decreased over these areas. There is convincing evidence linking the formation of lipofuscin to lipoperoxidation damage. In vitro experiments demonstrate that LF shows toxic and phototoxic effects and serves as a source of free radicals. Recently a major retinoid component of human RPE lipofuscin has been identified: N-retinylidene-N-retinylethanolamine (A2-E). In human RPE cell cultures


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