Abstract
Age-related macular degeneration (AMD) is associated with multiple genetic and cellular defects which lead to a common endpoint, retinal degeneration. Aging and oxidative stress, significant features in the pathogenesis of AMD, are associated with an increase in damaged intracellular organelles and defective autophagy flux in a range of age-related and neurodegenerative diseases. Autophagy is a key process in the maintenance of cellular homeostasis that serves to remove dysfunctional organelles and proteins. Autophagy proteins are strongly expressed in the retina and there is now strong evidence that mitochondrial damage and defective autophagy are a feature of the aging retina and that this is further exacerbated in AMD. It is apparent that autophagy makes a significant contribution to lipofuscin accumulation in the RPE. Pharmacological manipulation of autophagy may offer an alternative therapeutic target in AMD.
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