Age-related macular degeneration (AMD) is one of the most severe vision-threatening diseases. Wet AMD, caused by choroidal neovascularization (CNV), progresses rapidly, while dry AMD, characterized by neural retinal atrophy followed by choroidal vascular atrophy, progresses slowly. In addition to systemic risk factors, such as a high body-mass index (BMI), smoking, hypertension, and atherosclerosis, light-induced local oxidative stress and inflammation promotes AMD. CNV can be induced by multiple pathways. The accumulation of lipofuscin, a product of the undigested outer segments of photoreceptor cells, causes chronic local inflammation. Extracellular lipoprotein deposits, which contain pro-inflammatory components, such as complement, can trigger local inflammation. A single nucleotide polymorphism (SNP) in some genes; i.e., complement factor H (CFH) and excision repair cross-complementing rodent repair deficiency complementation group 6 (ERCC6), which induce local inflammation, is a risk factor for AMD. Two treatments, photodynamic therapy (PDT) and anti-vascular endothelial growth factor (VEGF) therapy, have been approved worldwide to cause the regression of CNV. In addition, the suppression of CNV progression combined with retinal neural protection by anti-oxidative reagents such as lutein/zeaxanthin and/or docosahexaenoic acid / eicosapentaenoic acid (DHA/EPA) is a promising prospective therapeutic approach. This is the subject of an ongoing prospective, randomized, double-blind, multicenter clinical trial, the Age-Related Eye Disease Study 2 (AREDS2). In addition, molecular and biological analyses in animal models have provided data supporting this anti-oxidant therapy.