17– 20 Pathological studies in AMD have also demonstrated the accumulation of lipids in Bruch’s membrane similar to the atherosclerotic changes of cardiovascular disease 21– 23, suggesting that statins might have an effect on AMD. 16 However, this class of drugs has exhibited unexpected anti-inflammatory, antioxidative, and anti-angiogenic effects. 15 The main role of statins is to inhibit 3-hydroxy-3-methyl-glutaryl-CoA reductase in the liver, down-regulating lipid metabolism. Statins, or 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors, currently the most commonly prescribed lipid-lowering class of drugs, 14 are proven to lower serum lipids and reduce cardiovascular morbidity and mortality. 7– 11 This potential inflammatory pathway is further supported by the statistically significant association of elevated serum C-Reactive Protein (CRP) with AMD in the Women’s Health Study, Rotterdam Study, and AREDS. 6 The association of genetic polymorphism in the complement pathway involving complement factor H and many other complement factors suggest that local or systemic inflammatory pathways may also be important in the pathogenesis of AMD. The use of antioxidant vitamins and minerals, known as the Age-Related Eye Disease Study (AREDS) supplement, reduces the risk of progression to late AMD, suggesting that oxidative stress may play a role in AMD. Associated risk factors include increasing age, cigarette smoking, hypertension, increased body mass index, lower educational level, presence of lens opacities, and others 2– 5. Age-related macular degeneration (AMD), a progressive disease that results in central vision loss, is the leading cause of blindness in persons over the age of 60 years in the United States.
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