Age-related macular degeneration (AMD) is one of the leading causes of adult blindness in the developed world. AMD accounts for over half the cases of adult blindness and twenty percent of the cases of low vision (Congdon, 2004, Figure 1). It already affects over 8 million Americans, and is expected to increase as the population ages (Friedman, 2004). Therefore, understanding this widespread disease and finding new and effective treatments will be critical for managing the health of an elderly population.
AMD is the most prevalent form of photoreceptor degeneration, which is a set of diseases characterized by death of the photoreceptor cells as either a primary or secondary event (Wright, 2010). As noted in a review by de Jong, the progression of AMD and the serious symptoms of the later stages of the disease appear to be linked to a disruption in the function of the RPE and Bruch’s membrane. The drusen deposits can promote a local inflammatory response, thereby leading to invasion of the retina by immune cells, like macrophages and dendritic cells. These inflammatory cells can release cytokines and angiogenic factors, which can go on to mediate chronic inflammation. This response can ultimately damage the cells of the RPE and Bruch’s membrane, thereby threatening the health of the photoreceptors (de Jong, 2006). In addition, oxidative stress of the RPE has also been implicated as an important factor in the development of AMD (Thurman, 2009). Finally, as a multifactorial, age related disease, AMD can be influenced by several environmental factors. Both smoking and excessive exposure to light can lead to inflammatory responses and the formation of reactive oxygen species, thereby leading to damage of the RPE (de Jong, 2006).