Age-Related Macular Degeneration

What is Age-Related Macular Degeneration?

Age-related macular degeneration, commonly referred to as AMD, is a retinal degenerative disease that causes a progressive loss of central vision. AMD is the most common cause of blindness in individuals over the age of 55 in developed countries. More than 10 million people in the United States have AMD.

The retina is packed with photoreceptors, the cells that enable us to see. Photoreceptors convert light into electrical impulses, which are transferred to the brain via the optic nerve and converted into the images we see. The macula is a small region in the center of the retina that’s rich in cones, the photoreceptors that enable a person to perceive fine details (e.g., read, recognize faces), colors, and objects in daylight or lighted conditions. Central vision loss from AMD occurs when cone photoreceptors in the macula degenerate.

The greatest risk factors for AMD are aging and smoking. An unhealthy diet and unprotected sunlight exposure can also increase AMD risk.  Genetics is also a risk factor.

Symptoms

People with AMD may first notice a blurring of central vision, especially during tasks such as reading or sewing. Also, straight lines may appear distorted or warped. As the disease progresses, blind spots may form within the central field of vision. In most cases, if one eye has AMD, the other eye has the condition or is at risk of developing it. The extent of central vision loss varies and can depend on the type of AMD — dry or wet.

Most people with AMD start off with the dry form. In many cases, people will not experience vision loss from the condition. In some cases, dry AMD can progress and cause varying degrees of central vision loss. Advanced dry AMD is sometimes referred to as geographic atrophy. 

The hallmark of dry AMD is the accumulation of tiny protein and fat deposits known as drusen underneath the retina. Many people have drusen, which do not affect vision. However, certain types of drusen may interfere with the health of the macula, causing progressive degeneration of the photoreceptor cells and vision loss.

About 10-15 percent of people with dry AMD will develop the wet form in one or both eyes. With wet AMD, abnormal blood vessels grow beneath the macula. These vessels leak blood and fluid into the macula and damage photoreceptor cells. Wet AMD often progresses rapidly and causes substantial loss of central vision, if left untreated.

Inheritance

Researchers have discovered that genetics can play a role in AMD risk. In 2005, three groups of researchers, including a team funded by the Foundation, discovered that a gene called Complement Factor H (CFH) is linked to at least 50 percent of all cases of AMD. Since that breakthrough, researchers have found several other genes linked to AMD. CFH and many of the other AMD genes are involved in the innate immune system, which fights off infection. Scientists believe that over activity of the innate immune system increases AMD risk.

While genetics can play a role in AMD risk, people with low risk genetics can still get the condition. Likewise, people with high risk genetics may not get AMD.

Treatment 

The Age-Related Eye Disease Study (AREDS) — a landmark investigation conducted by the National Eye Institute (NEI) — determined that a specific antioxidant supplementation can slow the progression of AMD. The AREDS2 formulation is an over-the-counter antioxidant supplement recommended for people who are at risk of developing more advanced forms of dry or wet AMD.

The AREDS2 formulation contains the following nutrients:

500 milligrams (mg) of vitamin C
400 international units of vitamin E
80 mg zinc as zinc oxide
2 mg copper as cupric oxide
10 mg lutein and 2 mg zeaxanthin

Several therapies are now available for the wet form of AMD. Most involve regular ocular injections to halt the growth of leaky, vision-robbing blood vessels.

EYLEA™ (alflibercept) — Regeneron’s wet AMD treatment, Eylea, blocks the development of unhealthy blood vessels underneath the retina. Regeneron reports that in clinical trials, Eylea treated wet AMD as effectively as Lucentis, but with fewer intraocular injections. Typically, patients are treated monthly with Eylea for three months and every other month thereafter. Eylea was FDA approved in 2011.

Lucentis™ (ranibizumab) — Developed by Genentech, Lucentis is effective in reducing the risk of losing vision from the abnormal blood vessel growth under the retina associated with wet AMD. The treatment was approved by the FDA and made available in 2006. A two-year study showed that 95 percent of people with wet AMD who received monthly injections of Lucentis experienced no significant loss in visual acuity from baseline. Genentech also reported moderate visual improvement in 24.8 percent of participants treated with a 0.3 mg dose of Lucentis and 33.8 percent of participants treated with a 0.5 mg dose.

A colorectal-cancer drug called Avastin® — a drug similar to Lucentis — has been used “off-label” by some ophthalmologists to treat wet AMD. The NEI completed a large-scale, two-year clinical study comparing Avastin and Lucentis. Results of the study showed that the drugs were similar in safety and efficacy.

Clinical Trials

View a list of current clinical trials, many made possible by Foundation support.

AMD page at www.ClinicalTrials.gov.