Authors' recommendations: Age-related macular degeneration (AMD) is the most common cause of blindness in the elderly. AMD is more common in white populations, although reported population-based frequencies are not entirely consistent. The incidence of AMD increases with age; while prevalence in individuals age 55 to 64 years is 0.2%, this rate increases to 13% in those older than 85 years of age. AMD is characterized by the presence of drusen—accumulations of lipids, proteins, and minerals that appear as white-yellow deposits in the retinal pigment epithelium of the eye. AMD may be divided into three categories based on the risk of vision loss. In early AMD, many small or intermediate-size drusen are present, with no evidence of advanced AMD. Intermediate AMD is diagnosed when drusen are larger but there is still no evidence of advanced AMD. Advanced AMD includes either geographic atrophy (GA) or neovascular AMD. Geographic atrophy, commonly called "dry AMD," features areas of total loss of retina, subepithelial blood vessels, and retinal pigment epithelium. In choroidal neovascular (CNV) AMD, also called "wet AMD," disease process begins as GA but shifts to growth of new blood vessels (neovascularization), which may bleed or leak fluid and cause retinal detachment. CNV comprises two-thirds of late AMD cases and is responsible for 90% of AMDrelated blindness. Approximately 8 million Americans have early AMD; in more than a million of these individuals, disease will progress to an advanced stage within the next 5 years. The extent and type of drusen present, along with hypo- or hyperpigmentary changes, are typically associated with risk for AMD disease progression. Risk factors for AMD include smoking, cataract surgery, family history of AMD, high body mass index (BMI), hypertension, and increased plasma fibrinogen. AMD prevention focuses on management of modifiable risk factors. Nutritional supplementation with antioxidant vitamins and zinc has shown some success in AMD risk reduction; however, this treatment is not recommended for smokers due to the association of beta-carotene with increased risk of lung cancer. Treatment options for AMD include laser photocoagulation, photodynamic therapy, and vascular endothelial growth factor (VEGF) inhibitors. Without treatment, both CNV and GA can lead to significant vision impairment, although progression of CNV is faster and may be more severe than GA. Two common genetic variants, p.Tyr402His (Y402H) in the complement factor H (CFH) gene and p.Ala69Ser (A69S) in the age-related maculopathy susceptibility 2 (ARMS2) gene, have been linked to development of AMD. While CFH p.Tyr402His is hypothesized to interrupt normal function of the complement cascade and ARMS2 p.Ala69Ser is thought by some to affect mitochondrial homeostasis, the purported pathogenic mechanisms of these variants in relationship to AMD are not clear.

Project Status: Completed

Year Published: 2012

URL for published report: The report may be purchased from:http://www.hayesinc.com/hayes/crd/?crd=13981

English language abstract: An English language summary is available

Publication Type: Not Assigned

Country: United States

Organisation Name: HAYES, Inc.

Contact Address: 157 S. Broad Street, Suite 200, Lansdale, PA 19446, USA. Tel: 215 855 0615; Fax: 215 855 5218

Contact Name: saleinfo@hayesinc.com

Contact Email: saleinfo@hayesinc.com

Copyright: 2012 Winifred S. Hayes, Inc