Over the past decade, our understanding about what causes different vision problems has dramatically improved, as has the sophistication of the technological tools and techniques available to help us solve those problems. Today, three cutting-edge methods of treating blindness—treatments that were scarcely imaginable even just a few years ago—are currently either in the experimental phase, or already available for use. Could a cure for blindness be far behind? Read on to learn more about these amazing biotech innovations.
1. The bionic eye
What is it?—Approved by the FDA in 2013, the Argus II is the first commercially available “bionic eye” in the United States. A kind of retinal prosthesis system, the Argus II is essentially a substitute eye.
What condition does it target?—Functioning as a retinal replacement, the Argus II targets conditions like retinitis pigmentosa, an inherited vision disorder that destroys the retinal cells responsible for detecting light and transmitting signals to the brain; in other words, the cells that allow the brain to process as images the light that we see.
How does it work?—Through a complicated surgical procedure, doctors insert the Argus II retinal implant into the patient’s eye. The other piece of equipment that allows the patient to “see” is a pair of high-tech sunglasses fitted with a small video camera with an attached video-processing unit. These glasses capture an image—just as a functioning eye would capture an image—and transmit a corresponding signal to the retinal implant. The implant then transmits electric pulses, bypassing the patient’s damaged photoreceptors, to those retinal cells that are still healthy. Stimulated by the electric pulses, these cells transmit the message to the brain that there is an image it should “see,” and thanks to this received message, it does.
This treatment approach is based on the flexibility and plasticity of the brain, which has significant capacity for learning and adapting to changing conditions. Weekly training sessions with the Argus II bionic eye are necessary, but gradually the brain adapts to this new way of “seeing.”
2. Stem cell injections
What is it?—The cells in our eye responsible for bringing nutrients to the retina are called retinal pigment epithelial (RPE) cells. Injections of stem cells, which have the ability to develop into any type of human cell, can therefore be used to replenish and replace damaged RPE cells.
What condition does it target?—Macular degeneration is the leading cause of vision loss in people over 60 years of age, though it can affect young people as well. In this condition, the RPE cells that feed the retina deteriorate; eventually, the retina dies, and thus the eye loses its ability to process light and transmit the signals necessary for seeing to the brain.
How does it work?—In a lab dish, harvested stem cells are treated with compounds that encourage them to develop into RPE cells. Doctors then inject a patient’s eye with these converted cells, up to 150,000 of them, and they continue to grow and develop; eventually, these stem cells should be able to serve as fully functional replacements for a patient’s original RPE cells.
Some researchers have compared the process of stem cell injections with the action of reseeding a dead patch of lawn with new grass seed—a helpful image to illustrate the idea of new growth replacing old.
3. Gene therapy
What is it?—This experimental treatment uses nonmutated genes that produce a protein that the photoreceptors in the eye need in order to work. As with the stem cell therapy, these genes are injected into the eye.
What condition does it target?—Some genetic conditions, including an early-childhood blindness disorder known as Leber congenital amaurosis (LCA), involve a genetic mutation that interferes with the proper functioning of the eye’s photoreceptors. Gene therapy techniques are designed to overcome the effects of the mutation by giving photoreceptors another way to access the protein they need. Genetic conditions of this kind are fairly rare; LCA, for example, affects around 3,000 people in the US.
How does it work?—Because the genetic mutation found in patients with LCA means, essentially, that the eye’s photoreceptors are not receiving the necessary instructions to do their job, other genes must be sent in to take over the role of giving directions. To get these genes into the eye, doctors inject a patient’s eye with a harmless virus carrying healthy, nonmutated genes. Once these genes are in the retina, vision gradually improves over time. However, a study from 2013 showed that the improvement isn’t permanent for all patients, and that further photoreceptor deterioration can continue even after the gene therapy injections. Nevertheless, researchers believe that even temporary vision improvement is a major step forward, and further experiments with this therapy are currently underway.