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Synopses of Research Articles Pinpointing the Earliest Defects in Age-Related Macular Degeneration DOI: 10.1371/journal.pmed.0030038 In the developed world, age-related macular degeneration (AMD) is the most common cause of blindness in later life—in the United States, for example, it affects around 15 million people. Early signs of AMD in the retina are pigmentation and soft drusen deposits of protein, fat, and cellular debris. Advanced AMD was previously classifi ed into wet and dry types; dry AMD, now known as geographic atrophy (GA) or atrophic AMD, occurs as the light-sensing cells (photoreceptors) in the macula break down. Wet AMD, now known as neovascular or exudative AMD, is caused when abnormal, fragile blood vessels grow under the macula, underneath the retina. These blood vessels often leak blood, lipid, and fl uid, which lift the macula. Late (sight-threatening) AMD is found in about 2% of all people over 50 years of age, and the incidence of the disease rises with age, occurring in 0.7%–1.4% of people aged 65–75 years, and in 11%–19% of people over 85 years of age. The neovascular form can rapidly lead to severe blindness, whereas the atrophic form progresses more slowly. Although age is the DOI: 10.1371/journal.pmed.0030038.g001 main risk factor for AMD, hypertension, smoking, and a family history of AMD also increase risk of developing the disease. Fundus images of A, normal macula; B, macula with confl uent soft Previous genetic linkage studies have suggested that a locus drusen C, macula with dry AMD D, macula with wet AMD. on the long arm of Chromosome 1 was involved in AMD’s pathogenesis. Further studies, then, refi ned these analyses and showed that a variant in one gene, Complement Factor H (CFH), CFH is a serum glycoprotein that controls the function of the was present more frequently in people with advanced AMD