Vitamin and mineral supplementation
The age related eye disease studies 1 and 2 (AREDS) showed that those with bilateral early or intermediate AMD, or intermediate AMD in one eye and advanced AMD in the other eye may benefit from specific vitamin and mineral supplementation. The specific vitamins and minerals in AREDS-1 are vitamin C (500 mg), zinc (80 mg), vitamin E (400 IU), copper (2 mg) and beta-carotene (15 mg). In the AREDS-2 formulation, lutein (10 mg) and zeaxanthin (2 mg) replaced beta-carotene due to the risk of lung cancer in smokers taking beta-carotene. These specific micronutrient supplementations were associated with a lower risk of progression to more severe forms of AMD and greater visual acuity at 5 years. There is no evidence that micronutrient supplementation prevents AMD progression in those with severe disease or prevents disease onset in those without AMD. Dry AMD
There is no cure for dry AMD. While there is increasing academic and pharmaceutical interest in developing complement inhibitors to treat ophthalmic inflammation, with several clinical trials underway for dry AMD, the first such agent to complete Phase 3 trials in AMD (the anti-factor D agent, lampalizumab) did not significantly improve the rate of disease progression. Nevertheless, strategies targeting different aspects of the complement system are ongoing. Wet AMD
Ranibizumab, aflibercept, brolucizumab and faricimab are approved VEGF inhibitors for the treatment of CNV in wet AMD. All three drugs are administered via intravitreal injection, meaning they are injected directly into the eye.
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".