Age-related macular degeneration (AMD) is a significant source of morbidity in aging adults. The damage to the macula and vision loss in advanced forms of wet AMD stems from choroidal neovascularization that originates in the choroid and proliferates through breaks in the Bruch membrane. Although inhibitors of angiogenesis have been a recent advance in the treatment of AMD associated with neovascularization, these agents do not appear to cure the condition. Rather, antiangiogensis agents halt or slow progression of AMD in most cases. The development of additional treatments to provide more effective disease control may depend on addressing several pathophysiologic processes simultaneously. The search for more effective treatments will require a better understanding of the different physiologic processes involved with this disease process.