Once the optic nerve that’s responsible for sight is damaged, it’s impossible to see again. At least that’s been the dogma. But a group of U.S. scientists has upended that thinking and helped mice with destroyed optic nerves to see again. It does not have immediate implications for humans yet, but it points researchers in promising new directions.
Andrew Huberman, an associate professor of neurobiology at Stanford University, and his team describe their advance in a study published in Nature Neuroscience. To learn about the way vision nerves grow, they crushed the optic nerve in one eye of mice. Once destroyed, the long finger-like extensions sent out by nerve cells from the eye to the brain start to shrivel, eventually severing any connection to the brain and resulting in blindness. Huberman and his colleagues, however, found that a combination of visual stimulation of the nerve, along with nerve-growing chemicals, can rescue these extensions, called axons, and coax them to stretch out again. Not only that, but the axons are able to find their appropriate connections to the correct sight-dedicated parts of the brain to restore vision. Mice with similar damage to the nerve that didn’t receive the treatment did not show much regrowth of the axons.
About three weeks after the optic nerves in the mice were damaged, the researchers saw evidence of axons extending back into the brain from the eye, something that previous efforts to regenerate eye nerves haven’t done with much reliability. The combination of keeping the damaged but remaining axons stimulated, by exposing the mice to bars on a screen that are moving in different directions, and the nerve growth factors lead to a 500-fold increase in axon regrowth. Granted, not all of the axons managed to sprout again, but those that did were able to do so with impressive speed and distance to reach the brain.
When the researchers conducted four different tests to verify how much of the regrowth contributed to actual restoration of vision in the animals, the animals passed two of the tests that detected large objects and movement.
“For the longest time people in the field wondered if neurons could regenerate and form the correct patterns to connect to the brain, and we found that they did,” says Huberman.
The most compelling finding is that the study suggest that once nerves are coaxed to grow again, they retain the instructions to find their proper connections in the brain’s visual center. If nerves growing toward the brain are like visitors to New York’s Grand Central Station, these nerves are like well-equipped travelers with maps and specific instructions for finding their destination. “It means that neurons remember the way home; they never forget,” says Huberman.
That’s encouraging him and his team to start considering how to translate the results to treat blindness in people. Keeping the axons stimulated by exposing them to stimuli is an easy first step; if these axons are kept alive, then they have a chance of regrowing again, as the mouse study showed. And now that it’s possible to push those axons to grow long enough to reach the brain, there is hope that some people with diseases like glaucoma, for example, might be able to retain their vision if they keep their compromised axons stimulated enough, and then eventually treat them with nerve growth factors.
That may be a few years away yet for people, but, Huberman is hopeful. “I want to see something positive in humans within five years,” he says.
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