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Age-Related Macular Degeneration: A Leading Cause of Blindness among Older Adults

Robert E. Coffee, MD, MPH, Clinical Instructor, Jules Stein Eye Institute, David Geffen School of Medicine, University of California, Los Angeles, USA.
Tara A. Young, MD, PhD, Assistant Professor, Jules Stein Eye Institute, David Geffen School
of Medicine, University of California, Los Angeles, USA.

Age-related macular degeneration (AMD) is the leading cause of blindness among older adults in North America. This article reviews the clinical spectrum, risk factors, pathophysiology, and potential therapeutic options for this disease. Despite significant advances in the treatment of certain forms of AMD, there is currently no cure for this degenerative condition. The substantial personal, social, and economic burden of AMD requires that those who provide care to older adults have a general understanding of this cause of blindness. It is important for the ophthalmologist and primary care physician to address modifiable risk factors for the progression of AMD such as poor cardiovascular status and smoking, which may worsen visual loss. In addition, educating patients and their families regarding risk factors and potential treatment options may greatly benefit those affected by AMD.
Key words: blindness, geriatric, age-related macular degeneration, choroidal neovascularization, ranibizumab, bevacizumab.

Introduction
Age-related macular degeneration (AMD) is a significant cause of blindness among older adults. The functional centre of the retina, known as the macula, is affected in this condition. Macular vision is important for both reading and facial recognition. While diagnosed and treated primarily by ophthalmologists, AMD can have a profound personal, social, and economic impact. Therefore, it is important that the geriatrician or general practitioner have an understanding of this disease and its implications for older adults. This article reviews not only the epidemiology, genetics, pathophysiology, ophthalmic manifestations, natural history, and treatment considerations for AMD, but the personal, social and economic impact of this disease as well.

Epidemiology
Age-related macular degeneration has traditionally been classified into two categories: atrophic (or dry, geographic, nonexudative) AMD and exudative (or wet, neovascular) AMD. The more common form is atrophic AMD, which comprises approximately 90% of individuals affected with AMD.1 Symptoms of atrophic AMD may range from no symptoms to a reduction in contrast sensitivity to gradually reduced central visual acuity, which may in some cases be severe. Exudative AMD often causes a sudden decrease in central vision ranging from new distortion to profound loss of central vision. The prevalence of visually significant AMD increases with age and is present in approximately 9% of adults aged 52-85 years.2 This makes AMD the most common cause of blindness in the developed world among older adults. Both genders and various ethnic groups are affected by AMD with relatively similar frequencies.

Genetics
A hereditary component to AMD has long been suspected due to the common occurrence of AMD in families. Progress in genetic studies of AMD, such as family based linkage analyses and case-control association studies, have brought increasing awareness to the hereditary nature of AMD.3 For example, variants in the complement factor H gene and LOC387715 have consistently been shown to be major risk factors for AMD. The practice of genetic testing for AMD is still in its infancy and generally controversial because of the wide overall prevalence of these genes in the general population.

Pathogenesis
The initiating cause of AMD remains unknown. However, the final common pathway involves damage to the retinal pigment epithelial cells and underlying connective tissues beneath the neurosensory retina. The accumulation of metabolic byproducts of aging cells4 and chronic microvascular ischemic insults5 have been hypothesized as the fundamental abnormalities in AMD. While recently published research has implicated chronic inflammation in the pathogenesis of AMD, other mechanisms such