After patients develop cataracts, the leading cause of blindness, vision can often be restored through surgery. But little can be done to restore vision in patients with glaucoma, the second-leading cause of blindness, or other forms of optic-nerve damage.

Researchers led by Andrew Huberman, PhD, associate professor of neurobiology, have restored partial vision for the first time in mice whose optic-​nerve cables were completely severed. They coaxed the cables, which convey visual information from the eye to the brain, to regenerate, retrace their former routes and re-establish connections with the appropriate parts of the brain.

Information is transmitted from the eye to the brain via the retinal ganglion cells, whose long, wirelike axons travel down the optic nerve and then fan out to more than two dozen areas of the brain. Like most axons in the mammalian central nervous system, retinal axons do not regenerate, so damage means permanent vision loss. One reason: a set of molecular interactions called the mTOR pathway, which enhances axons’ growth, winds down after early development.

When the researchers biochemically activated the mTOR pathway in mice, exposed them to constant visual stimulation in the form of a moving black-and-white grid and covered their undamaged eye to encourage them to use their damaged eye, substantial numbers of axons regrew and migrated to their appropriate destinations in the brain. The mice were able to use that eye to discern an expanding dark circle — analogous to an approaching bird of prey — but not for tasks that required finer visual discrimination.

Huberman is the senior author and Jung-Hwan Albert Lim, a graduate student at the University of California-San Diego, is the lead author of the study, which was published in the August 2016 issue of Nature Neuroscience.

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