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There is no cure for glaucoma, the second-most common cause of blindness (after cataracts), but a new study offers hope that it might not always be so. In lab mice, combining two very different therapies let the animals see again — at least partially.

Why it matters:

Glaucoma is caused by damage to the optic nerve, which connects the eye to the brain. The optic nerve is part of the central nervous system, which is notorious for failing to recover from injuries. That’s why spinal neurons that get crushed in an accident don’t bounce back.


Scientists have put a lot of effort into figuring out how to make neurons recover, and are still searching for a cure for diseases that result from nerve damage, like spinal trauma or glaucoma.

But in a Stanford University study published Monday in Nature Neuroscience, researchers found that a combination of two treatments, visual stimulation and molecular manipulation, makes the severed optic nerve of lab mice partially grow back.

The nitty gritty:

The retina, a thin layer of cells lining the back of the eye, converts light into electrical signals and sends them to the brain so we can see. These signals pass through the optic nerve, which is made up of over a million retinal ganglion cells (RGCs) — tiny orbs with long tails called axons. The axons form a web of wires reaching from the eye to parts of the brain specializing in different aspects of vision, like the color blue, a moving car, or the distance between your foot and the sidewalk.


The RGCs are the only bridge between the eye and the brain. If the RGCs are injured, the result is irreversible vision loss — even if the eye and the brain are functioning normally.

“Think of the brain as a computer, the eye as a smart phone, and the axon as the USB cable that connects them,” said neurobiologist Andrew Huberman, the study’s senior author.

Huberman and his team crushed the RGCs of lab mice and then exposed them to one or a pair of treatments: a virus that promotes the growth of cells, and exposing them to videos of moving black and white lines.

Mice who experienced only visual stimulation had their RGCs partially grow back, though their axons did not get long enough to reach the brain — a result that previous studies have also found.

On its own, injecting a virus that reactivates a growth pathway called mTOR also got the RGCs to regenerate partially. But again, they did not make the full distance to the brain.

When the two therapies were combined, however, not only did the RGC axons grow long enough to make it back to the brain, but they also found and reconnected with their correct targets.

There are about 30 types of RGCs, and each sends its axons to a different and specific location in the brain. “It’s a very intricate wiring system,” explained Huberman. The fact that the axons found their way back to the right place was “incredibly reassuring,” he said.

The researchers blinded the mice in only one eye, and observed that the RGCs regenerated the most when they sewed shut the other eye, forcing the weaker eye to work harder.

What they’re saying:

“This is an important step forward,” said neuroscientist Mark Bear of the Massachusetts Institute of Technology, a leading researcher on the brain and visual system who was not involved in the new study.

It’s “a very significant advance in the regeneration of axons … and very relevant to conditions that result from trauma to the optic nerve or spine,” he said.

This discovery may, in the future, help treat patients suffering from other diseases or injuries in which cells of the central nervous system are damaged — something that scientists previously thought was impossible.

The results of the study are especially promising because visual stimulation is a relatively simple procedure that is already being tested on humans,, said Dr. Jeffrey Goldberg, professor and chair of ophthalmology at the Byers Eye Institute at Stanford University, who was not involved with the study.

But it may take some time until the other part of the therapy, activating the mTOR pathway to regenerate nerve cells in the eye, can be widely used on humans.

But keep in mind:     

Not all the RGCs of the optic nerve recovered. “The mice went from being completely blind to being able to perceive the motion of large objects and the direction of movement,” said Huberman.

For a mouse, this means being able to flee or freeze if it spots the shadow of a hungry cat or looming hawk. For a blind person, it would mean being able to navigate large objects — but not read or reach for small objects.

Also, there’s a long way to go from mice to humans.

A certain catchy nursery rhyme for decades tricked even neuroscientists into thinking mice are blind. “If you told someone 10 years ago that you were going to study vision in mice, they would have laughed,” said Huberman.

But mice can see — far better than previously thought — and researchers have found that studying vision in mice has numerous advantages.

The bottom line:

A two-pronged therapy to regenerating brain cells in mice showed early promise, offering the possibility that researchers might some day be able to restore some vision in humans or give paralyzed people back some mobility.