Blind World

Regenerating the retina; Early results suggest that transplants of fetal retinal cells might halt and even reverse the loss of sight in the millions of people with degenerative eye diseases.

February 1, 2003.

By Duncan Graham-Rowe,
New Scientist.

TRANSPLANTS of fetal eye tissue seem to have improved the vision of two out of four people with a degenerative eye disease. It is too early to be sure the improvements are real and lasting, but on the strength of the results the team pioneering the surgery has asked regulators for permission to carry out further operations.

Before the experimental surgery on her left eye a year ago, Elisabeth Bryant, who is 63, could barely see anything with it. "Now I can see people's eyes, noses and mouths when they're sitting across the room from me." Like the other patients in the trial, she has advanced retinitis pigmentosa, a hereditary disease that causes degeneration of the retina. It affects around 1 in 3500 people in Western countries. There is a danger of creating false hope, warn experts such as Alan Bird at Moorfields Eye Hospital in London. But the potential benefits of the procedure are too high not to continue, he says. The real pay-off could be a treatment for common diseases, such as age-related macular degeneration, which is responsible for half the blindness in Britain. "It's an enormous problem. And it seems to be increasing and occurring at an even younger age," Bird says.

Over the past few decades, many attempts have been made to treat failing sight by transplanting various kinds of retinal cells. But the transplants are often rejected or fail to improve vision. Robert Aramant and Magdalene Seiler at the Doheny Eye Institute in Los Angeles think these obstacles can be overcome by transplanting a double layer of cells from the retinas of aborted fetuses.

In their treatment, surgeons insert 2-millimetre squares of tissue, which include the supporting layer of epithelial cells as well as the top layer of light-sensing rods and cones, behind the degenerating retina. The idea is that the epithelial cells, which nourish and support the light-sensing cells, will help halt the progress of any disease, while the retinal cells will replace those already lost.

Using intact sheets is important, says Aramant, because it preserves the circuitry between the light-sensing cells. And fetal cells are better tolerated by the immune system, so patients do not have to take immunosuppressive drugs.

In rats, the transplanted cells not only survive but also form connections with the remaining cells in the retina. But the team has had to rely mainly on patients' subjective reports to assess the results in people. This doesn't really count in science, Aramant admits.

It is also difficult to tell if the reported improvements in vision are due not to the donor cells but to a short-term process called the "rescue effect". A disturbance to the eye can trigger the release of growth factors that save diseased or damaged cells. But the effect does not last. "Any surgical intervention has the possibility of inducing short-term improvements," says John Greenwood at the Institute of Ophthalmology in London, who is experimenting with implanting stem cells into the retina.

So the team will be watching patients like Bryant closely to see if their vision continues to improve. "It's possible that this is a rescue effect, but we are hoping that it is from connections to the remaining healthy cells in the retina," says Norman Radtke at the University of Louisville in Kentucky, the eye surgeon who carried out the operations.

The team now want to treat people with less advanced retinitis pigmentosa, as they believe the transplants should be more effective if given at an earlier stage.

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