The photoreceptor cells of the retina capture light and transform it into a signal which can be interpreted by neurons in the brain. Photoreceptors reside in the deepest layer of the retina, and include the cone cells (which give us colour vision) and the rods (which give us our night vision). The remaining retinal layers and parts of the brain work-up those signals to create our visual perception. Inside each of the 200 million rod and cone cells are stacks of hundreds of light-absorbing layers. To keep in top shape a substantial proportion of older layers get discarded and replaced every day. This causes a potential garbage recycling problem.  In early AMD this garbage begins to accumulate, forming deposits called drusen that sit within the retinal layers. 

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As AMD progresses these drusen become larger and more numerous. At certain point patches of retina go into one of two states: death of the retinal layers called geographic atrophy (GA), or growth of malformed and destructive leaky blood vessels called neovascular AMD (nAMD).  These are sometimes called Dry and Wet AMD, although older nomenclature also refers to the earlier drusen-only phase as Dry AMD.

 

There are treatments for nAMD but little for GA. The ratio of nAMD to GA patients is about 2:1. As the name implies the risk of AMD rises with age, especially over age 65. By 2030 there are expected to be about 1.44 million Australians with early AMD, and 215,000 who are visually impaired in both eyes by later-stage AMD.  Vision ACTion and its partners are developing diagnostics and therapeutics for both nAMD and GA, and we are exploring the factors that determine progression from early to late-stage disease.