Age-related macular degeneration (AMD) is a common disorder in the aged people that affects the central region of the retina, which is called macula. AMD is the leading cause of legal blindness in people older than 65 in the developed world. AMD is characterized by very typical retinal pathologies including drusen, retinal pigment epithelium dysfunction, retinal degeneration (geographic atrophy) and choroidal neovascu-larization. Recent studies reveal that oxidative stress and inflammation are significantly linked to the pathogenesis of AMD. Retina is especially susceptible to oxidative stress by following reasons: 1) photoreceptors contain polyunsaturated fatty acids, 2) retina is exposed continuously to light, 3) its oxygen consumption is high, 4) it contains chromopheres which react with light and produce reactive oxygen species (ROS). Moreover, ran-domized, prospective, placebo-controlled study in United States showed that high-dose supplementation of beta-caroten, vitamin C, vitamin E, copper, and zinc significantly slowed the progression of the disease and visual deterioration in patients with AMD. Mice deficient of Cu, Zn-superoxide dismutase showed typical features of human AMD, suggesting that oxidative stress scavenger may play a critical role in the prevention of age-related retinal degeneration. Obesity and inflammatory biomarkers are significantly associated with the risk of AMD, which possibly indicates that AMD is considered as a consequence of disturbance of homeo-stasis, such as metabolic syndrome. Recent genetic studies showed genes related to immune system via complement are associated with AMD, which revealed that inflammatory reactions are causally linked with the pathogenesis of AMD. Recently, the inhibitor of angiotensin II type 1 receptor reduced the volume of experimental CNV after laser burn, suggesting that angiotensin II type 1 receptor blockade be a novel therapeutic strategy as a preventive treatment for AMD. Further research is necessary to invent mechanism-based therapies forAMD.
2006 by The Japanese Society of Inflammation and Regeneration