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Scientists Find Protein in Limb-Nerve Repair

  • Jessica Berman

Images of axon regeneration in mice two weeks after injury to the hind leg’s sciatic nerve. On the left, axons (green) of a normal mouse have regrown to their targets (red) in the muscle. On the right, a mouse lacking DLK shows no axons have regenerated,

Images of axon regeneration in mice two weeks after injury to the hind leg’s sciatic nerve. On the left, axons (green) of a normal mouse have regrown to their targets (red) in the muscle. On the right, a mouse lacking DLK shows no axons have regenerated,

Researchers have identified a protein that's essential for the regrowth of nerves responsible for movement and sensation in injured limbs. They hope the finding might some day make it possible to repair crippling damage to other parts of the central nervous system.

Scientists have long known that severed nerves in the arms and legs have the ability to regenerate after they have been been surgically reattached. But until now, the mechanisms underlying that regrowth have been poorly understood.

Scientists at Washington University School of Medicine in St. Louis, Missouri, discovered that a protein, called dual-leucine zipper kinase (DLK), plays a key role in repairing the long, thin nerve fibers, or axons, that extend several meters from the nerve cell body within the spinal cord to so-called peripheral nerves in the limbs.

Developmental biology professor Aaron DiAntonio, who studies how the nervous system responds to injury, says that when a peripheral nerve is damaged, DLK signals the nucleus of its nerve cell - the nerve's "brain" in effect, at the other end of the axon in the spinal cord - to turn on its regeneration program.

In their experiments with mice, DiAntonio and his team discovered that when DLK is not present, the injury message is not relayed to the nerve cell body, its regeneration mechanism is not turned on and axonal regrowth is stalled.

DiAntonio believes this new understanding of DLK's role opens up a range of possibilities for repairing nerve damage not just in the limbs but throughout the central nervous system.

"The first place one might be able to apply it would be in the peripheral nervous system. So, we just have to turn on something that already exists," DiAntonio says. "Bigger picture, longer term, of more importance if it worked, would be in the central nervous system, where first we would have to ask, 'Is it just a non-funtional nervous system?' And if it is, how would we turn it on?"

The researcher notes that the DLK nerve repair mechanism does not work in other nerves throughout the central nervous system, since damage to the spinal cord usually results in paralysis. Instead, the researcher believes, the central nervous system's role may be simply to monitor and relay DLK's damage signals from peripheral nerves.

"And if that's the case, then if we can - and we don't know how to do this yet - but if we could figure out how to turn on this injury-signalling system now that we've identified it, we can look to see if it's in the central nervous system and are there ways to activate it," he says.
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