This over-production causes excess blood vessel formation in the choroid region (the choriocapillaris), which is a major cause of wet AMD. However, the RPE has a G-protein coupled receptor, GPR143, that is activated by its ligand, extracellular L-DOPA. Activation of GPR143 reduces RPE secretion of VEGF. Activation of GPR143, with the reduction in VEGF, may be the main protective role of L-DOPA against wet AMD. Management
Treatment of AMD varies depending on the category of the disease at the time of diagnosis. In general, treatment is aimed at slowing down the progression of AMD. As of 2018, there are no treatments to reverse the effects of AMD. Early-stage and intermediate-stage AMD is managed by modifying known risk factors such as smoking cessation, management of hypertension and atherosclerosis and making dietary modifications. For intermediate-stage AMD, management also includes antioxidant and mineral supplementation. Advanced-stage AMD is managed based on the presence of choroidal neovascularization (CNV): dry AMD (no CNV present) or wet AMD (CNV present). No effective treatments exist for dry AMD. The CNV present in wet AMD is managed with vascular endothelial growth factor (VEGF) inhibitors. Daily use of an Amsler grid or other home visual monitoring tools can be used to monitor for development of distorted vision, which may be a sign of disease progression.
The three loci where identified gene variants are found are designated:

Complement Factor H (CFH) on chromosome 1 at location 1q31.3
HTRA serine peptidase 1/Age Related Maculopathy Susceptibility 2 (HTRA1/ARMS2) on chromosome 10 at location 10q26
Complement Factor B/Complement Component 2 (CFB/CC2) on chromosome 6 at 6p21.3

Specific genes
Polymorphisms in genes for complement system proteins: Variation in the genes for the complement system proteins factor H (CFH), factor B (CFB) and factor 3 (C3), among others, are strongly associated with a persons risk for developing AMD. CFH is involved in inhibiting the inflammatory response. The mutation in CFH (Y402H) results in reduced ability of the protein to localise to and protect tissues such as the retina from complement overactivation. Absence of the complement factor H-related genes R3 and R1 protects against AMD. Two independent studies in 2007 showed a certain common mutation Arg80Gly in the C3 gene, which is a central protein of the complement system, is strongly associated with the occurrence of AMD. The authors of both papers consider their study to underscore the influence of the complement pathway in the pathogenesis of this disease. In two 2006 studies, another gene that has implications for the disease, called HTRA1 (encoding a secreted serine protease), was identified. Six mutations of the gene SERPING1 (Serpin Peptidase Inhibitor, Clade G (C1 Inhibitor), Member 1)  are associated with AMD. Mutations in this gene can also cause hereditary angioedema. Fibulin-5 mutation: Rare forms of the disease are caused by genetic defects in fibulin-5, in an autosomal dominant manner. In 2004, Stone et al.