Therapy of Nonexudative Age-Related Macular Degeneration

Abstract

Age related macular degeneration (AMD) is the leading cause of blindness among adults over the age of 65 in the Western world. The prevalence of AMD is expected to increase dramatically, from 1.75 million in 2000 to 2.95 million in 2020, due to the rapidly aging population. Given the large and now increasing burden of disease, the identification of modifiable risk factors and new avenues for preventive treatment has become increasingly important. The pathogenesis of macular degeneration is multi-factorial with genetic, environmental, and physiologic components. The retina is uniquely susceptible to oxidative damage, given its high metabolic activity and daily exposure to light. In addition, the presence of large numbers of lipids with double bonds makes it an ideal target for reactive oxygen species. The increasing incidence of macular degeneration with advancing age may be related to gradual dysfunction and degeneration of retinal tissues as oxidative damage accumulates. This cumulative damage may result in physiologic dysfunction, in addition to impaired auto-regulation with restricted exchange and processing of nutrients and metabolic byproducts with progressive disease. Nutrients which may modulate this oxidative damage include lutein, zeaxanthin, beta-carotene, C, E, and B vitamins, and zinc. A growing body of scientific evidence also implicates inflammatory processes in the pathogenesis and progression of macular degeneration. Clinical evidence suggests a role for a combination of antioxidants in reducing progression of AMD and a potential role for omega-3 fatty acids and macular xanthophylls in the prevention and treatment of macular degeneration. The Age Related Eye Disease Study 2 (AREDS2) will further examine the role of these micronutrients in the treatment of AMD.