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The Role of Inflammation and Infection in Age-related Macular Degeneration

Age-related macular degeneration (AMD) affects more than 1.75 million individuals in the United States and is the leading cause of blindness in persons over the age of 65 in Western countries. The earliest signs of AMD include drusen and changes in the retinal pigment epithelium (RPE). Late changes include geographic atrophy and choroidal neovascularization (CNV). AMD is broadly classified into dry and neovascular forms. Dry AMD is characterized by the presence of drusen (localized deposits between the RPE and Bruch’s membrane) and geographic atrophy (areas of localized RPE cell death with overlying photoreceptor atrophy), whereas neovascular AMD is characterized by CNV. CNV accounts for 10% of cases of AMD but advanced AMD (geographic atrophy involving the macular center and neovascular AMD) causes 90% of visual loss. AMD is a complex disorder that is associated with a number of demographic, genetic, and environmental factors. Increasing evidence has suggested a role for local and systemic inflammation in the pathogenesis of this disease. Risk factors associated with AMD include advanced age, cigarette smoking, race, family history, body mass index (BMI), underlying cardiovascular disease, and systemic inflammatory markers such as C-reactive protein (CRP). Some of these risk factors may predispose individuals to AMD by inflammatory mechanisms. Genetic factors may also lead to AMD by inflammatory mechanisms. Recently, several groups have determined that a variant of the gene encoding complement factor H (CFH), the Tyr402His polymorphism, is strongly associated with the development of AMD in whites.5–7