Today, most people who develop wet age-related macular degeneration (AMD) can retain much of their vision thanks to the advent of three treatment options, all administered through repeated ocular injections.

The alternatives are: Lucentis, a monthly treatment approved by the FDA in 2006; Avastin, an equally effective, low-cost, off-label alternative to Lucentis; and Eylea, which was approved by the FDA in 2011, and is as effective as Lucentis, but with fewer treatments.

These therapies are having a dramatic impact on vision around the world. For example, Danish researchers reported earlier this year that the rate of legal blindness from wet AMD in their country decreased by 50 percent from the year 2000 to 2010, with most of the reduction occurring after 2006, when Lucentis and Avastin became widely used.

That’s the good news.

The not-so-good news is that, even though these treatments work, wet AMD invariably returns in all patients, usually within a few months after the treatment is stopped, and retreatment (i.e., additional ocular injections) is necessary. Some retinal doctors continue monthly treatment for the life of the patient even after the leaky blood vessels that cause vision loss from wet AMD are no longer apparent. And as you might imagine, or know firsthand, ocular injections are inconvenient, can cause some discomfort and carry small risks.

However, there are potentially better options on the horizon. Three companies — Oxford BioMedica, Genzyme, and Avalanche — are conducting early-stage clinical trials of gene therapies that could potentially halt wet AMD for several years, perhaps a lifetime, through a one-time ocular injection. These treatments work by delivering copies of a gene to the retina that operate like little biotech factories, providing continual release of a protein that prevents the growth of vision-robbing leaky blood vessels. While these gene therapies are in safety studies for now — we won’t know if they prevent vision loss for perhaps a few years — we’re excited about their potential.

What is also exciting for me is that the technologies used to deliver the therapeutic gene to the retina — manmade viruses — are very similar to those developed earlier by Foundation-funded researchers for the treatment of rare diseases like Leber congenital amaurosis (LCA), retinitis pigmentosa, Usher syndrome, choroideremia, and Stargardt disease.

One of the big challenges in treating rare inherited retinal degenerations is that there are so many of them — several dozen, in fact. But, fortunately, many of the treatment approaches we fund apply to many diseases. So, while a therapy for a rare disease like LCA might initially target a few hundred or a few thousand people, it might ultimately help millions. When it comes to fighting blindness, we are all in it together.