Treatment of age-related macular degeneration: beyond VEGF

Abstract

Current therapy for age-related macular degeneration (AMD) shows a dramatic change from clinical practice a decade ago. While the first pharmacologic treatment, verteporfin photodynamic therapy (PDT) slowed disease progression, newer anti-vascular epithelial growth factor (VEGF) therapies have also shown vision improvement in many patients. Combination therapies (PDT + steroid + anti-VEGF) have shown some promise, particularly in certain classes of disease. Genetic studies have identified common gene variants in the complement factor H gene that confers susceptibility to AMD, and treatments targeting the complement pathway are being explored. Another area of research is directed at the components of Bruch membrane; studies of changes in the elastic fibers and collagen within Bruch may yield drug targets for prevention and halting of disease progression. Finally, studies in photoreceptor apoptosis have identified the role of cytokines, such as monocyte chemotactic protein 1, tumor necrosis factor α, and interleukin 1β, associated with photoreceptor cell death and should be pursued as potential therapies to improve vision outcomes in neovascular AMD. Today's research into the biology of AMD will lead us to better treatment and perhaps even preventive measures in the decades ahead.