The 20th century was undoubtedly an era of tremendous medical progress. If anyone doubts it, just consider that in one short century, the average life expectancy for Americans made its biggest jump in history—from 47 to 77. Life-saving procedures like blood transfusions, heart bypass surgery and organ transplants became commonplace, and in the industrialized world, infectious diseases were all but wiped out. The focus of medicine throughout history has been to save lives that would otherwise be cut short, and that effort is still very much alive. But more of the medicine of the 21 st century is turning its attention to improving the quality of life for the millions of older people who have far outlived their parents but who suffer from crippling disabilities.
Take, for example, the 3.6 million Americans who have a blinding eye disease called age-related macular degeneration (AMD). AMD is the number one cause of legal blindness, which doesn't sound so bad until you realize that we are talking about an irreversible loss of sight that cannot be repaired or corrected with glasses. Those who have macular degeneration have to learn to live without the most important part of human vision, what ophthalmologists call central vision.
Central vision, or the part of vision at the very center of our visual field, is the only part capable of the sharp, clear focus we rely on to do practically everything—read a book, write a check, drive a car, get dressed in the morning. AMD obliterates central vision by destroying the light-sensing cells of the macula, the crucial area at the very center of the retina. Once these cells are lost, they are gone forever, and along with them goes all but our fuzzy, out-of-focus peripheral vision. Anything a macular degeneration patient looks directly at vanishes into a dark blur, making it a struggle to perform almost any daily function without assistance.
The challenge faced by scientists in their quest to cure AMD is that our bodies don't replace the dead cells of the retina at anywhere near the level needed to restore lost vision. At the same time, scientists and engineers have made unheard-of strides in the creation of ever smaller and more powerful computer chips, wireless technologies and microelectronics. So what about applying some of these technologies to providing patients with artificial vision? In the world of cutting-edge research, a handful of scientists are trying to do just that.
One possible source of sight may be through the implantation of a special microchip into the human retina, a technology being pioneered by Dr. Mark Humayun at the University of Southern California 's Doheny Retina Institute. So far experimentation with a retinal chip has brought modest results for two blind patients, allowing them to distinguish light from dark, read large letters and make out the outlines of large objects like the walls of a corridor.
The chip works through a rather complex apparatus made up of several components. First, the patient must wear a special pair of glasses that are fitted with a miniature camera. Through wireless technology, the camera sends light signals to a small receiver which has been positioned behind the patient's ear. The receiver passes the signal along to a tiny wire implanted under the skin of the scalp. From there, it is transmitted to the retinal chip implant, which then sends it along the optic nerve to the brain. Amazingly, this allows the blind patient to experiences a crude form of vision.
The makers of the chip technology admit that the system is physically cumbersome and has a long way to go before it can produce the kind of high-resolution vision blind patients hope for. It certainly doesn't allow for seeing fine details or the subtle beauties of a sunset. But these efforts provide proof of principle that providing the brain with visual signals from sources external to the body can actually produce sight.
Dr. Humayun says that, ultimately, the technology depends on the brain's ability to make sense of the chip's electronic signals. It will not work in patients who were born blind, because the brain has to have been trained to “see” through previous experience with sight. This makes it highly suitable, once the bugs are worked out, for victims of macular degeneration, who mostly begin to lose sight after the age of 50. The researchers hope that, eventually, these patients can have a tiny camera implanted in the eye itself, where it will transmit directly to a retinal chip that will pass messages on to the brain. They caution, however, that it will be several years before some form of this technology becomes widely available.
Considering the workings of the experimental retinal chip only highlights the efficient, and miraculous, phenomenon of human sight. What if we could get around nature's limits by simply supplying the living parts that are missing—in this case, light-sensing retinal cells—in eyes that have lost them because of disease? This is what Dr. Henry Klassen, now at the University of California-Irvine is trying to do. It turns out that the eye does generate some new retinal cells, just far fewer than are needed. What if we could learn how the eye gives birth to retinal cells by isolating and harnessing the stem cells, or parent cells, that give rise to them?
Dr. Klassen has already crossed two important hurdles in his search for a way to replenish the eye's light-sensitive cells. First, he discovered through experimentation with mice that the eyes of adult mammals actually produce small numbers of stem cells that can be nurtured in lab dishes into becoming the all-important rods and cones of the retina. But retinal cells are nerve cells, and nerve cells are useless unless they can make connections and communicate with other nerve cells. No one knew whether transplanted nerve cells would integrate themselves into the network of connections in an adult retina, which is comparable to the brain's neural network. But Dr. Klassen's experiments in transplanting new retinal cells into mice showed that they could.
Now Dr. Klassen is working with the retinal tissue of donated human eyes to try to separate the stem cells that are the progenitors of retinal neurons. The next step will be to learn how to make these cells flourish in cell cultures so that sufficient numbers of them can be produced for transplantation. If this can be done in a reliable fashion, it could have a tremendous impact on treatments for macular degeneration and other blinding diseases like diabetic retinopathy. It means that stem cells could be taken from the patient's own eyes so that there is no chance of a genetic mismatch. Then new retinal cells grown from the patient's own genetic blueprint could replenish a depleted retina, in effect resetting the clock on a lifetime of sight.
Scientists are quick to caution that work like the above is still in its infancy, and the road to discovery is often littered with obstacles. But if the last few years of medical progress are any indication, there is reason to hope that the profound visual disability experienced by millions today could soon become a thing of the past.