Questions & Answers

Researchers continue to explore environmental, genetic and dietary factors that may contribute to developing AMD. New treatment strategies are also being explored, including retinal cell transplants, drugs to prevent or slow down the progress of the disease, radiation therapy, gene therapies, a computer chip implanted in the retina (may help simulate vision) and agents to prevent the growth of new blood vessels under the macula.

All wet AMD is considered advanced; however, the dry form of AMD has three stages:

• Early AMD - patients have several small drusen or a few medium-sized drusen. There is no vision loss or symptoms at this stage.
• Intermediate AMD - patients have many medium-sized drusen or one or more large drusen. Some people may need more light for tasks such as reading. A blurry spot may appear in the center of the visual field.
• Advanced AMD - patients exhibit a large number of drusen deposits and a breakdown of RPE and photoreceptor (light sensitive) cells and supporting tissue in the retina. A large blurry spot occurs in the center of the visual field and can become larger and darker, eventually causing a complete loss of central vision.

Yes, some people with macular degeneration also develop Charles Bonnet Syndrome (CBS) and hallucinate. Some eye diseases prevent normal nerve impulses from reaching the brain, and it is believed that spontaneous, brain-generated nerve activity may cause visual hallucinations. CBS appears to be more common in women than men and is more likely to occur if both eyes are affected by disease. The hallucinations are normally complex and can include detailed patterns or fully formed images such as animals, people, faces or scenery. Patients know that the hallucinations are not real. These images are not associated with any other sensory (e.g., sound or odor) hallucinations, nor are they delusions. The hallucinations may last for seconds or for most of the day. They tend to disappear when people close their eyes. CBS may last for days or even years, but can be managed by educating the patient and reassuring him or her that the images are a result of eye disease, not a mental disorder.

• View a video of neurologist and author, Dr. Oliver Sacks, discussing Charles Bonnet Syndrome.

It is possible to develop AMD in only one eye. However, as the disease progresses, both eyes may become affected. If advanced AMD occurs in one eye, there is a much greater risk of developing advanced AMD in the other.

To help diagnose AMD, an eye care professional will perform a dilated eye exam to view the retina and optic nerve for damage, a visual acuity test to measure sight from various distances and a fundoscopy to examine the back of the eye. If wet AMD is suspected, fluorescein angiography, in which dye is used to detect leaking blood vessels, may also be performed. The patient might be asked to look at Amsler grid; if the straight lines on the grid appear wavy or distorted, AMD may be developing.

AMD is a common eye disease associated with aging that gradually destroys sharp, central vision. The retina is the very thin tissue that lines the back of the eye and contains the light-sensing cells that send visual signals to the brain. Sharp, clear, 'straight ahead' vision is processed by the macula, which is the central part of the retina. When the macula is damaged, many daily activities such as driving, reading and recognizing faces become increasingly difficult.

Age-related macular degeneration (AMD) typically affects individuals over 50 years old. Scientific evidence shows that genes may play a role in the development of nearly three out of four cases of this devastating eye disease.

Several genes are believed to be strongly associated with the risk of developing AMD:

• Factor H and Factor B genes are responsible for proteins that help regulate inflammation in the part of the immune system that attacks diseased and damaged cells. According to study results published in 2006 by Columbia University, 74 percent of AMD patients carry certain variants in one or both of these genes, and these may significantly increase their risk of developing it.
  
  
• PLEKHA1 – a gene located on chromosome 10; researchers believe it may increase the risk of developing AMD. Like Factors H and B, PLEKHA1 appears to be involved in the cellular processes related to inflammation.
  
  
• LOC387715 – A certain variation of this gene appears to increase the risk of developing AMD. This risk is further heightened if a person with this gene variation also smokes.
  
  
• HTRA1 – Scientists have identified a link between a mutation in this gene and the development of AMD. Specifically, the HTRA1 mutation is thought to be associated with the formation of drusen (yellow deposits of waste products under the retina that are often a sign of dry AMD), and may also promote the growth of fragile new blood vessels typical of wet AMD.
  
  
• Complement C3 – Researchers have found that a variant in this gene increases the risk of developing the wet and dry forms of AMD. This gene plays an important role in the immune system, leading scientists to believe that inflammation is a vital part of the AMD disease process.

Other gene candidates are being studied to determine their role in AMD. While there is definitely a strong genetic component to this disease, it is highly likely that its development is due to a combination of multiple factors including gene mutations or variations and environmental factors such as sunlight exposure, diet and smoking.

There are two forms of AMD: dry and wet. It is possible for a person to suffer from both forms, for AMD to affect one or both eyes, and for the disease to progress slowly or rapidly. Dry AMD may advance and cause loss of vision without turning into the wet form of the disease. However, it is also possible for early-stage dry AMD to change into the wet form of the disease.

Dry macular degeneration is the most common type of AMD. This form, in which the photosensitive cells of the macula slowly break down, is diagnosed in 85-90 percent of cases. Yellow deposits called drusen (extracellular waste products from metabolism) form and accumulate under the retina between the retinal pigmented epithelium (RPE) layer and the Bruch's membrane, which supports the retina. Drusen are often found in the eyes of older people, but an increase in the size and number of these deposits is frequently the first sign of macular degeneration. Over time, drusen are associated with deterioration of the macula and the death of RPE and photoreceptor cells, resulting in a blurring or spotty loss of clear, straight-ahead vision.

Wet macular degeneration occurs when abnormal blood vessels grow behind the macula as RPE and photoreceptor cells die. The Bruch’s membrane begins to break down, usually near drusen deposits, and new blood vessels grow. This growth is called neovascularization. These vessels are very fragile and can leak fluid and blood, resulting in scarring of the macula and the potential for rapid, severe damage. Straight-ahead vision can become distorted or lost entirely in a short period of time, sometimes within days or weeks. Wet macular degeneration accounts for approximately 10 percent of the cases, but it results in 90 percent of the cases of legal blindness. All wet AMD is considered advanced.