Rodent models offer the advantages of low cost, disease progression on a relatively quick time scale, and the ability to perform genetic manipulation. Models of AMD have been created in mice, rats, rabbits, pigs, and non-human primates. Second, anatomical differences between the species used for AMD models and the human retina have lent further complexity to the task. Oxidative stress, inflammation, and lipid and carbohydrate metabolism have all been implicated in the pathology of AMD. Rather than being caused by a single genetic defect, numerous genetic polymorphisms have been implicated in contributing increased risk for AMD. First, AMD is a complex process involving both genetic and environmental factors. Developing a model that mimics both the early and late features of AMD has been challenging due to several obstacles. As shown in Table 1, numerous models mimic several of the important pathological features seen in AMD, but none recreated all of its characteristics. The ideal model of AMD would be inexpensive, recapitulate the histological and functional changes, but evolve in a rapid time course to allow more efficient studies. Dry AMD is much more common than wet, but choroidal neovascularization (CNV) in wet AMD accounts for the majority of the vision loss ( Bressler et al., 1988).Īccurate animal models of a disease can assist greatly in the development of new therapies. AMD can progress to a “dry”, non-neovascular form leading to geographic atrophy of the retinal pigment epithelium (RPE), choriocapillaris, and photoreceptors, or to a more rapid “wet”, neovascular form, which occurs when new blood vessels invade from the choroid and penetrate Bruch's membrane resulting in vascular leakage, hemorrhage, and scarring.

AMD is a heterogeneous disease, which first manifests in the macula with the appearance of pigmentary changes and subretinal deposits called drusen. This article will review the diversity of animal models that exist for AMD as well as their strengths and limitations.Īge related macular degeneration (AMD) is the leading cause of blindness in the industrialized world of adults older than 65 years ( Klein et al., 2002). Models for induced choroidal neovascularization have served as the backbone for testing new therapies. However, these models have helped reveal the roles of chronic oxidative damage, inflammation and immune dysregulation, and lipid metabolism in the development of AMD. In spite of the large number of models developed, no one model yet recapitulates all of the features of human AMD. Models in mice, rats, rabbits, pigs and non-human primates have recreated many of the histological features of AMD and provided much insight into the underlying pathological mechanisms of this disease. AMD is a complex and heterogeneous disease that involves the interaction of both genetic and environmental factors with the unique anatomy of the human macula. The prevalence and need to develop effective treatments for AMD has lead to the development of multiple animal models.

Age related macular degeneration (AMD) is the leading cause of vision loss of those over the age of 65 in the industrialized world.

Animal age related conditions