One of the great challenges in neuroscience has been learning how to coax nerves to regenerate after injuries. Now scientists have shown that a newly discovered and highly potent growth-promoting molecule can regenerate the optic nerves of rats – and do so days after the nerves have been damaged.
Although still in its early stages, the research offers hope that one day a treatment can be devised for people who suffer damage to the optic nerve, which connects the eye to the brain. Furthermore, the work suggests that this growth factor may help with spinal-cord injuries as well.
Published in the journal Nature Neuroscience, the study found that rats’ optic nerves were stimulated to regrow by several millimeters, says Larry Benowitz, director of the Neuroscience Laboratory at the Children’s Hospital in Boston, who led the research.
The experiment involved placing a protein with previously unidentified growth-promoting properties into the eye fluid of rats whose optic nerves had been crushed three days earlier.
“This is not going to restore sight,” cautions Jerry Silver, a neuroscientist at Case Western Reserve University in Cleveland. “But it has opened up a new chapter in regeneration biology.” Not only does the research identify an entirely new growth-promoting molecule for nerves, which appears to be more potent than any other neurotrophic substances, says Silver, but it also explains the mechanisms involved.
The notorious reluctance of nerve fibers to heal themselves has left millions of people permanently impaired. And previous efforts to encourage these fibers to regenerate have had mixed results, says Martin Berry, a neuroscientist in the Molecular Neuroscience Group at the University of Birmingham, U.K.
Until now, the most promising regeneration had been achieved by both Benowitz and Silver independently, using an unlikely approach. “We had earlier found that when we caused an inflammatory reaction in the eye, it paradoxically stimulated nerves in the eye to go into a growth state,” says Benowitz. It was known that this odd effect was likely due to a type of white blood cell, called macrophages, secreting some unknown substance.
Working with colleagues from Harvard Medical School, the University of Missouri, and MIT, Benowitz has now shown, through a painstaking process of elimination, that the protein responsible is a small molecule called oncomodulin.