Lending credibility to this has been the discovery of disease-associated genetic polymorphisms in other elements of the complement cascade including complement component 3 (C3).A powerful predictor of AMD is found on chromosome 10q26 at LOC 387715. An insertion/deletion polymorphism at this site reduces expression of the ARMS2 gene though destabilization of its mRNA through deletion of the polyadenylation signal. ARMS2 protein may localize to the mitochondria and participate in energy metabolism, though much remains to be discovered about its function. Other gene markers of progression risk includes tissue inhibitor of metalloproteinase 3 (TIMP3), suggesting a role for extracellular matrix metabolism in AMD progression. Variations in cholesterol metabolising genes such as the hepatic lipase, cholesterol ester transferase, lipoprotein lipase and the ATP-binding cassette A1 correlate with disease progression. The early stigmata of disease, drusen, are rich in cholesterol, offering face validity to the results of genome-wide association studies. Stages
In AMD there is a progressive accumulation of characteristic yellow deposits, called drusen (buildup of extracellular proteins and lipids), in the macula (a part of the retina), between the retinal pigment epithelium and the underlying choroid. This accumulation is believed to damage the retina over time. Amyloid beta, which builds up in Alzheimers disease brains, is one of the proteins that accumulate in AMD, which is a reason why AMD is sometimes called "Alzheimers of the eye" or "Alzheimers of the retina".
Other symptoms of AMD include distortion of vision and blind spots (especially in and around the central visual field).Other signs and symptoms of macular degeneration include:

Distorted vision in the form of metamorphopsia, in which a grid of straight lines appears wavy and parts of the grid may appear blank: Patients often first notice this when looking at things like miniblinds in their home or telephone poles while driving. There may also be central scotomas, shadows or missing areas of vision
Slow recovery of visual function after exposure to bright light (photostress test)
Visual acuity drastically decreasing (two levels or more), e.g. : 20/20 to 20/80
Blurred vision: Those with nonexudative (wet) macular degeneration may be asymptomatic or notice a gradual loss of central vision, whereas those with exudative (dry) macular degeneration often notice a rapid onset of vision loss (often caused by leakage and bleeding of abnormal blood vessels). Trouble discerning colors, specifically dark ones from dark ones and light ones from light ones
A loss in contrast sensitivity
Formed visual hallucinations and flashing lights have also been associated with severe visual loss secondary to wet AMD Macular degeneration by itself will not lead to total blindness. For that matter, only a small number of people with visual impairment are totally blind. In almost all cases, some vision remains, mainly peripheral. Other complicating conditions may lead to such an acute condition (severe stroke or trauma, untreated glaucoma, etc.