**5. Dry AMD**

Toxic accumulations, either within the RPE cell or at the RPE-Bruch membrane interface, are the molecular hallmarks of dry AMD [18]. Dry AMD may be considered as a form of a metabolic storage disease; two approaches to preventing their formation or removing them after formation are attempts to prevent RPE damage. AMD and other neurodegenerative disorders occur when a particular cell or group of cells die. In this scenario, AMD might share some pathogenetic mechanisms with several common neurodegenerative diseases of aging, such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease in which mitochondrial defects, DNA mutations, impaired structural integrity, and defective mitochondrial function. Other toxins accumulate in AMD; an excessive amount of "lipofuscin," which is nondegradable debris that accumulates in the RPE with age, is associated with AMD. In the presence of light, lipofuscin forms ROS and is toxic to RPE cells [19–20].
