Dry age-related macular degeneration (AMD) is one of the major causes of blindness in the elderly population and it is the consequence of interactions of multiple factors. Although the pathogenesis of dry AMD hasn't been fully elucidated, much progress has been made in the genetics, inflammation, oxidative stress, aging of retinal pigment epithelium (RPE) cells and metabolic changes. Identification of dry AMD related genes and predisposing loci facilitates the development of risk evaluation of dry AMD. Presence of β-amyloid in the drusen implies similarities between AMD and other degenerative diseases. Dysfunction of complement system, discovery of Nod-like receptor family containing pyrin domain 3 inflammasome and the concept of parainflammation reinforce the role of inflammation. Oxidative stress, mitochondrial dysfunction and decreased autophagy capacity, which are related to aging of RPE cells, demonstrate the critical role of it and metabolic changes in the pathogenesis.
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