Age-Related Macular Degeneration
Also known as: AMD, ARMD, Macular degeneration
Overview
Age-related macular degeneration (AMD) is a progressive disease of the central retina and a leading cause of irreversible central vision loss in people over 50. It is divided into non-neovascular (dry) disease, marked by drusen and, in advanced form, geographic atrophy, and neovascular (wet) disease, in which choroidal neovascularization threatens rapid vision loss. Anti-VEGF therapy transformed the prognosis of wet AMD.
- Affects
- Central retina (macula)
- Forms
- Dry (non-neovascular), Wet (neovascular)
- Wet AMD therapy
- Intravitreal anti-VEGF
- Advanced dry
- Geographic atrophy
Key clinical points
- Dry AMD is far more common; wet AMD accounts for most severe, rapid vision loss.
- Drusen and pigmentary changes define early and intermediate disease.
- AREDS2 supplementation reduces progression risk in intermediate and advanced disease.
- Anti-VEGF injections are the mainstay for neovascular AMD, with newer agents extending treatment intervals.
- Complement inhibitors are now available to slow the growth of geographic atrophy.
Classification and staging
AMD is staged from early (medium drusen) to intermediate (large drusen and/or pigmentary changes) to advanced disease. Advanced AMD takes two forms: geographic atrophy, a well-demarcated loss of the retinal pigment epithelium and photoreceptors, and neovascular AMD, in which abnormal choroidal vessels leak or bleed beneath and within the retina.
OCT is the workhorse for detecting fluid and monitoring therapy, while OCT angiography and fluorescein angiography characterize neovascular membranes.
Risk factors and prevention
Age, smoking, family history, and genetic factors are the strongest risks; smoking cessation is the most impactful modifiable intervention. The AREDS2 formulation of antioxidant vitamins, zinc, lutein, and zeaxanthin reduces the risk of progression to advanced disease in patients with intermediate or advanced AMD in one eye.
Home monitoring for new distortion and prompt evaluation of sudden central visual changes support early detection of conversion to wet disease.
Treatment
Neovascular AMD is treated with intravitreal anti-VEGF agents, which stabilize and often improve vision. Newer higher-durability agents and treat-and-extend regimens reduce injection burden. Geographic atrophy, historically untreatable, can now be slowed with intravitreal complement inhibitors, though these do not restore lost vision.
Low-vision rehabilitation is an essential component of care for patients with established central vision loss.
Age-Related Macular Degeneration videos
Frequently asked questions
- What is the difference between dry and wet AMD?
- Dry (non-neovascular) AMD involves drusen and, when advanced, geographic atrophy, and progresses slowly. Wet (neovascular) AMD involves abnormal blood vessel growth that can cause rapid central vision loss and is treated with anti-VEGF injections.
- Do AREDS2 supplements prevent AMD?
- AREDS2 supplements do not prevent AMD from developing, but they reduce the risk of progression to advanced disease in patients who already have intermediate or advanced AMD.
- Can geographic atrophy be treated?
- Intravitreal complement inhibitors can slow the enlargement of geographic atrophy lesions, but no therapy currently restores vision already lost to atrophy.
References & further reading
Related conditions
Geographic Atrophy
Geographic atrophy (GA) is the advanced form of non-neovascular (dry) age-related macular degeneration, defined by sharply demarcated areas of loss of the retinal pigment epithelium, photoreceptors, and choriocapillaris. It causes progressive, irreversible loss of central vision, often sparing the fovea until late and producing dense scotomas that impair reading and face recognition. Complement inhibitors are the first therapies shown to slow GA lesion growth, though none restore vision already lost.
Clinical overviewRetinaDiabetic Retinopathy
Diabetic retinopathy is a microvascular complication of diabetes mellitus and a leading cause of vision loss among working-age adults. It progresses from non-proliferative changes—microaneurysms, hemorrhages, and exudates—to proliferative disease with neovascularization that risks vitreous hemorrhage and tractional detachment. Glycemic and blood pressure control plus timely screening are the foundation of prevention.
Clinical overviewRetinaRetinal Vein Occlusion
Retinal vein occlusion (RVO) is one of the most common retinal vascular disorders, caused by thrombotic obstruction of a retinal vein that leads to hemorrhage, macular edema, and, in ischemic cases, neovascularization. It is classified as branch or central depending on the site of occlusion. Vision loss most often results from macular edema, which is treated effectively with anti-VEGF therapy.
Clinical overviewRetinaDiabetic Macular Edema
Diabetic macular edema (DME) is the accumulation of fluid in the central retina due to breakdown of the blood–retinal barrier in diabetes, and it is the most common cause of vision loss in patients with diabetic retinopathy. It can occur at any stage of retinopathy. OCT has made diagnosis and monitoring precise, and anti-VEGF therapy is the first-line treatment for center-involving disease.
Clinical overview