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Some patients also lose daylight vision and go blind completely, because the color-sensing cone cells of their inner retinas slowly degenerate. But the disease doesn’t kill cone cells immediately; it first makes them nonresponsive to light. That means there is a window of time where the cone receptors are still there, but not functioning.
So scientists at the Friedrich Miescher Institute for Biomedical Research in Basel, Switzerland, attempted to reanimate diseased cone cells in mice. Using a virus already approved for human gene therapy, the researchers inserted a gene from a light-sensitive bacterium, Natronomonas pharaonis, into cone-cell DNA.
The gene is a blueprint for proteins that form passageways in cell membranes. When stimulated by light, those proteins open up and let negatively charged ions into the cell. When inserted in the mouse cell membranes, these proteins helped mimic the normal activity of healthy cones.
Not only did the restored cone cells respond to light, but they also sent signals to the brain so the mice could see.
“What was really astounding is that these cells that were blind for a while were still connected to the rest of the circuit,” says neurobiologist Botond Roska, who led the study.
But unlike healthy cone cells, the restored cone cells could not adapt to different light levels. The cells responded best to bright yellow light similar to sunlight at the beach, Roska says. In order for human patients to see in dimmer light, researchers would have to develop special glasses with light-sensing cameras to adjust the intensity of light projected to the patients’ eyes, he says.