Researchers at University of Utah have identified a worm gene that can be over-activated to speed damaged nerve cell regeneration.
The researchers said that their discovery is a step toward new treatments for nerves injured by trauma or disease.
"We discovered a molecular target for a future drug that could vastly improve the ability of a neuron to regenerate after injury," either from trauma or disease, says biology Professor Michael Bastiani, leader of the research team and a member of the Brain Institute at the University of Utah.
Study co-author and biology Professor Erik Jorgensen - the Brain Institute's scientific director - said: "In the future, we would like to develop drugs that could activate this chain of molecular events in nerve cells and stimulate regeneration of diseased and injured nerve cells. At this point, we can't do that. But this study gives us hope that in the future, we will have a rational approach for stimulating regeneration."
Bastiani said that an ability to stimulate nerve regeneration one day also may help treat multiple sclerosis, in which nerves are damaged by loss of their myelin coating.
He said that the study used nematode worms, which "have the same molecules performing similar functions in humans. We found a pathway that not only regenerates nerves in the worm but also exists in humans, and we think it serves the same purpose."
The core of the molecular chain of events involves four genes. The most important is dlk-1¸ which is known as a "MAP kinase kinase kinase" or MAPKKK.
When the researchers 'overexpressed' the dlk-1 gene in worms - making it more active than normal - broken nerves in the worms regenerated much more quickly than expected. When dlk-1 was blocked, regeneration did not occur.
Study co-author Paola Nix, a biology research associate, said: "The next thing to do would be to test this gene in [other] animals and eventually humans to see if it plays the same role."
The study is published in the Jan. 22 issue of Science Express, the online edition of the journal Science.