title: [Age-related macular degeneration - biology and treatment].
abstract: Age-related macular degeneration (AMD) is the main cause for legal blindness of the elderly in the industrialized world and due to the demographic changes of the Western societies the prevalence is expected to increase strongly. The late forms of this disease are differentiated into geographic atrophy and exsudative (wet) AMD, where vessels grow from the choroid into the retina. On a biological level, the most important structure ofAMD pathogenesis in the photoreceptor/retinal pigment epithelium (RPE)/choroid complex. The interaction of the components of this structure enables the photoreceptors to function. Age-related alterations of this complex play an important role in the development of AMD. The exact triggers for AMD onset, however, are not known. There are no available therapies for the early forms of AMD or for geographic atrophy. However, the exsudative form can be treated by inhibiting vascular endothelial growth factor (VEGF). The currently available therapeutics (ranibizumab, aflibercept, bevacizumab) show good results in the clinic, however, in order to uphold the therapeutic effect they have to be regularly injected into the vitreous body. The inhibitors differ on a molecular level as well as on a biological level concerning their interaction with retinal pigment epithelial cells.
authors.forename: Alexa
authors.initials: A
authors.lastname: Klettner
mesh_terms: D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000627:therapeutic use; D000068258:Bevacizumab; D006801:Humans; D008268:Macular Degeneration / Q000188:drug therapy* / Q000503:physiopathology; D000069579:Ranibizumab
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D000068258:Bevacizumab; D000069579:Ranibizumab