The miracle of biology

Huge progress has been made in restoring normal hearing to the deaf: within the last 40 years, scientists have developed prosthetic devices, called cochlear implants, which allow deaf people to communicate without lip reading or signing, and even to talk on the phone.

So why isn’t there something like this for the eye, to restore vision to the blind?

The most common causes of blindness arise from degeneration of the retinal cells that detect light, the photoreceptor cells. When these cells die, the remaining nerve cells in the retina survive for a while before they too die.

Several labs are building chips that can be inserted behind the retina, where the photoreceptor cells are in the normal eye (Tübingen, Tokyo Institute of Technology). These implants stimulate the surviving nerve cells, mimicking the photoreceptor cells.

Other labs want to tack (yes, tack) their implants onto the front of the retina (Harvard & MIT, John Hopkins & USC).

The visual scene is captured either by a camera attached to a pair of glasses, which transmits the signals to the implant in the eye, or by photocells on the chip itself.

Retinal implants are being tested in patients, with moderate success. Patients who were completely blind are able to make out bright light sources and some movement.

Great, right? Seeing vaguely is better than not seeing at all, and certainly makes daily life easier. But retinal implants may never advance to the level of the cochlear implants.

This is because the retina is far more complex than the cochlea. The cochlea pretty much just encodes frequency (pitch) and intensity (loudness). All the rest, including the location of a sound source, is processed in the brain. The retina, on the other hand, does a huge amount of processing before sending its signals to the brain.

Object location, brightness, orientation, motion, and color are all encoded in the retina. So the electrical signals that the retinal implant produces need to include all of this information. But retinal scientists are only just beginning to understand how all this works.

These problems may be solved eventually, and in the meantime, people with implants are happy to have 16-pixel vision.

But this month, Botond Roska, of the Institute for Biomedical Research in Basel, presented a brilliant new idea for restoring vision to the blind (Nature Neuroscience 11:667-675).

His idea was to confer the ability to detect light onto the nerve cells which survive after the photoreceptor cells die. His team did this by introducing the gene for a light-sensitive protein into a specific group of nerve cells in the retina.

This protein builds channels in the membrane of the cell. When the channel is stimulated by light, it opens, allowing charged particles to flow into and out of the cell. This flow of charges is an electrical signal, and it is the same as the signal that these cells produce in the normal retina when they are stimulated by photoreceptor cells.

Dr. Roska’s team tested their idea in blind mice. When these mice were treated with the gene for the light-sensitive channel protein, their vision was restored with relatively high acuity.

This project is in its infancy, and there are a lot of problems to be worked through. For example, normal room lighting is too dim to stimulate the channels, so some sort of amplifying system will have to be worked out.

It may be another 50 years before scientists are able to restore vision of reasonable quality to blind people, but I’d be willing to bet that when it does happen, it’ll be by gene targeting and not by retinal implantation.