(AMD) is a deterioration of the retina and choroid that leads to a substantial loss in visual acuity (sharpness of vision). AMD is the leading cause of significant visual acuity loss in people over age 50 in developed countries.

In early stages, AMD may have no symptoms at all. When the disease progresses, the symptoms are:

• Distortion (warping) of straight lines
• A decrease in the intensity or brightness of colors

As the macular degeneration progresses, AMD symptoms include:

• A gradual or sudden loss of central vision, or
• Dark, blurry areas in the center of vision

Causes: The exact cause of AMD is unknown, but the condition develops as the eye ages. There are 2 types of AMD: non-neovascular or dry AMD; and neovascular or wet AMD.

In early stages of dry AMD, the hallmark is drusen—pale yellow lesions formed beneath the retina. Drusen are usually harmless, but as they accumulate, dry AMD can progress. Atrophic areas (areas of atrophy or wasting) in the retina also may develop; if the atrophic area is significant and with sharp borders, it is termed geographic atrophy (GA).

GA is the advanced form of dry AMD, which is frequently associated with loss of central vision.

In wet AMD, there is a sudden or gradual decrease in visual acuity, blind spots in the center of vision, and distortion of straight lines. The hallmark of wet AMD is choroidal neovascularization (CNV).

CNV occurs when abnormal blood vessels grow beneath the retina; these can bleed or leak and cause a distortion of the retina’s structure. Ultimately, the CNV can turn into a disciform scar that replaces the normal architecture of the outer retina and leads to permanent loss of central vision.

Risk Factors

• Age—the strongest risk factor
• Family history of AMD
• Caucasian race
• Cigarette smoking

Possible risk factors:

• Female gender
• High blood pressure
• Higher level of education
• High cholesterol
• Light iris color
• Sunlight exposure
• Far-sightedness
• Low dietary fish intake
• Cardiovascular (heart) disease

Disease features related to AMD may be found in the retina and in the layers beneath it. According to these abnormal findings, AMD is classified as dry or wet.

An AMD diagnosis is made by a clinical examination performed by a retina doctor at a slit lamp and by using several types of imaging, including:

• Dye angiography
• Optical coherence tomography (OCT)
• 'Non-invasive' OCT angiography (OCTA)
• Autofluorescence (AF) imaging

Wet-AMD treatment has been revolutionized in recent years after the discovery of vascular endothelial growth factor (VEGF), a family of compounds in the body. VEGF regulates the growth of abnormal new blood vessels in the eye—known as neovascularization—that can lead to wet AMD.

Anti-VEGF drugs have been developed to help stop neovascularization and preserve vision for AMD patients.

Wet AMD cannot be cured, but its progression may be blocked with the use of intravitreal (in-the-eye) anti-VEGF injections. Local anesthetic eye drops are given before the injections to numb the eye and minimize discomfort.

There are 3 anti-VEGF treatment regimens:

1. Pro re nata (PRN) or “treat and observe”—patients are treated with three initial monthly injections, followed by treatment as needed.
2. “Treat and extend”—after 3 initial monthly injections, the time between treatments is gradually increased until wet AMD is stabilized.
3. Monthly injections.

Before the first anti-VEGF drugs were introduced, wet-AMD patients were treated with laser photocoagulation or photodynamic therapy (PDT).

Anti-VEGF drugs have greatly improved wet-AMD treatment since 2005; patients today have a much better chance of maintaining their central vision so they can read, drive, recognize faces, and live normal lives.

Although patients with either form of AMD can experience a severe decrease in visual acuity, they will almost never be completely blind.