Journal
VETERINARY PATHOLOGY
Volume 47, Issue 3, Pages 396-413Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/0300985809359598
Keywords
Bruch's membrane; choriocapillaris; complement; degeneration; macula; retinal pigment epithelium
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Funding
- National Institutes of Health [K01 RR16090-01A2]
- Claude D. Pepper Older Americans Independence Center at Yale University School of Medicine [P30-AG21342]
- NATIONAL CENTER FOR RESEARCH RESOURCES [K01RR016090] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P30AG021342] Funding Source: NIH RePORTER
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Age-related macular degeneration (AMD) is a degenerative condition that begins in Bruch's membrane and progresses to involve the retinal pigment epithelium and ultimately the overlying photoreceptors. The only required etiologic factor is age, and AMD is regarded as the leading cause of blindness in individuals older than 65 years. AMD results from variable contributions of age, environment, and genetic predisposition. Many loci are linked to AMD; in the majority of cases, the disease is associated with polymorphisms within these genes, rather than mutations that ablate gene function. The etiologic complexity of AMD is reflected by the paucity of animal models that entirely replicate the human disease. This review compares the salient anatomy of the primate and rodent retina, particularly in the light of AMD pathology. It next discusses prevailing hypotheses explaining how AMD may develop. These include the role of complement activation and macrophage chemotaxis in AMD, molecular mechanisms of choroidal neovascularization, and the roles of oxidative damage and lipid metabolism. Finally, the article gives an overview of spontaneous and induced nonhuman primate models and describes relevant mouse models in the context of each pathogenetic mechanism.
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