Age-related macular degeneration (AMD) has a number of characteristic features including late onset and accumulation of deposits (drusen) below the retinal pigment epithelium on Bruch's membrane in the macula. A progressive increase in these deposits (in some individuals) leads to macular blindness, following either the local loss of the retinal pigment epithelium (geographic atrophy) or the hemorrhage of new blood vessels that originate in the choroid and invade the compartment between the photoreceptors and retinal pigment epithelium (choroidal neovascularization). Over the last few years a number of mouse models for AMD have been described that replicate some of the changes manifest in the human disease. This chapter begins with a description of the hallmarks of AMD, discusses some of the ideas about the underlying mechanisms and then summarizes the features of AMD found in experimental animals that are purported to model this disorder.Key words: Age-related macular degeneration (AMD), Drusen, Bruch's membrane, Geographic atrophy, Choroidal neovascularization, AMD animal model Age-related macular degeneration (AMD) constitutes a major cause of legal blindness in the elderly population of developed countries. Millions of individuals over 55 years of age are blind from AMD in Europe and North America with over 300,000 new AMD cases presenting annually (1, 2). In some individuals, in addition to the normal age-related thickening of Bruch's membrane, focal accumulation of debris on Bruch's membrane causes nodular elevations of the RPE that are recognized in an eye exam as drusen (3-5). Clinicians have long recognized that the presence of drusen in the macula, their size, density, and the area encompassed by these deposits represent early stages in the AMD disease process. While the initial drusen deposits are not associated with 1. Age-related macular degeneration: The Human Condition