Science & Research

Yes, gene therapy holds much promise for treating degenerative diseases such as macular degeneration; however, it is very complicated. Thus far, scientists have only identified some of the genes that increase the risk of developing macular degeneration. Also, the exact causative genes and contributing factors may differ from person to person, so there would likely be no single universal treatment that would work for everyone. Additionally, an effective means (both for patient comfort/protection as well as for cost effectiveness) for delivering the treatments to the patients would have to be worked out. Hence, in theory, gene therapy sounds ideal; however, much work remains before it will become common practice in patient treatment.

I am not certain how New York compares with other states in terms of securing funding for and/or executing clinical trials for macular degeneration research, so I cannot comment specifically on this. However, I do know that there are many physicians/researchers in New York that are actively engaged in pioneering research on macular degeneration and that conduct clinical trials. The New York Eye and Ear Infirmary is one example of a site that conducts a number of clinical trials in ophthalmology. On their website, you will find several current clinical trials for macular degeneration being conducted in New York. For a more comprehensive overview of other clinical trials throughout the nation, please visit the National Eye Institute’s website and search their clinical trials database.

The visual prognosis for branch retinal vein occlusions is highly dependent on the location of the affected vessel in your retina. Branch retinal vein occlusions often result in chronic retinal edema that is difficult to treat. If the macula and fovea (the part of the retina responsible for clear central vision) are involved, the visual prognosis can be poor. You mentioned that you have been treated with laser and steroid treatments. More recently, anti-VEGF agents, such as Avastin, have been shown to be useful in improving visual acuity and decreasing macular edema in branch retinal vein occlusions.

Currently, there is no reported toxic level of lutein in the literature, and the potential benefit of using lutein for age-related macular degeneration has not been established yet in a prospective clinical study. Supplemental lutein for dry macular degeneration is currently being studied in the ongoing AREDS 2 trial. Enrollment for this clinical trial ended in June of 2008 and patients are being followed for 5 years.

Enablex has not been reported to have any effect on macular degeneration. However, as a muscarinic agonist, it can potentially precipitate an attack of acute glaucoma in patients who are predisposed to this condition.

Cystoid macular edema (CME) has been associated with high doses of niacin. Reports in the literature indicate that this ocular side effect may be dose-dependent. Most patients with niacin-induced CME were taking relatively high doses, between 3-6 grams of niacin per day. The effect appears to be reversible upon discontinuation of the drug.

Laser photocoagulation is no longer the first line therapy for wet age-related macular degeneration (AMD). With the recent development of anti-VEGF agents such as Lucentis and Avastin, intravitreal* injections of the above medications are often the initial treatment for neovascular (wet) AMD. That said, the success rate of laser treatment is variable from patient to patient, depending on the location of the abnormal blood vessel growth and the type of laser (photocoagulation vs. photodynamic therapy).

*Intravitreal refers to the eye's vitreous humor, which exists between the lens and the retina.

• View an "Anatomy of the Eye" medical illustration.

Depending on the extent of scar tissue that has formed and its location, laser treatment is an option in some cases. It is true that many researchers are trying to find ways to prevent macular degeneration from occurring, but there are also researchers working diligently to explore better treatment options for patients currently affected by the disease.

While I’m not sure if this idea has been explored scientifically or not, it is important to note that as macular degeneration progresses, so does the damage to the rods and cones. In fact, the rods and cones begin to deteriorate as more and more damage occurs to the retinal pigmented epithelium (RPE), which is responsible for photoreceptor cell nourishment and removal of waste products. As such, even if there was an effective way to double the amount of light available for processing by cone cells, patients with advanced macular degeneration have fewer cone cells available to process information, which would likely limit any potential benefit.