In addition, thinning of the choroid is linked to the development of outer retinal atrophy after regression of subretinal drusenoid deposits. Primary MA (without prior wAMD) that follows age-related choroidopathy is well demarcated and precedes atrophy and photoreceptor loss, tending to occur in patients aged >80 years and in association with reticular pseudodrusen and/or glaucoma. MA may occur at any point in AMD and arise by several distinct mechanisms (Table 1). Patients receiving anti-VEGF agents must be assessed for overall risk of MA, and there is an unmet medical need to prevent the development of MA without undertreating wAMD. Evidence suggests that subretinal fluid (possibly indicative of residual VEGF activity) may play a protective role. These patients are characterized as having a pre-existing thin choroid (age-related choroidopathy), suggesting that the choroidal circulation is unable to respond to increased VEGF expression. Patients with type III macular neovascularization (retinal angiomatous proliferation) have a particularly high risk of MA. For example, excessive blockade of VEGF through intense use of anti-VEGF agents may accelerate the development of MA. Therefore, it is important to identify risk factors for the development of MA in patients with wAMD. However, recent evidence suggests that anti-VEGF treatment may play a role in the development of MA. The standard of care for wAMD is treatment with anti-vascular endothelial growth factors (VEGFs).

MA causes irreversible vision loss and currently has no approved pharmacological treatment. Late AMD can be classified into exudative (commonly known as wet AMD ) or dry AMD, both of which may progress to macular atrophy (MA). Age-related macular degeneration (AMD) is a leading cause of blindness.

Vegfr2 wet amd genetic link