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New Hope for Spinal Injuries
Treatment with a protein is found to guide nerve regeneration
By Lindsay Peterson
When spinal nerves are damaged, there is little that doctors can do. But now Tufts researchers have found that when a certain protein is applied to the damaged nerves, they seem to reconnect to the spinal cord, signaling a potential treatment breakthrough for the 450,000 people in the United States who live with these debilitating injuries.
Eric Frank, professor and chair of physiology at Tufts School of Medicine, focuses his research on injuries to the brachial plexus, a network of nerves that send signals from the brain to the shoulder, arms and hands. When these nerves are crushed in a traumatic injury, the electrical signaling between the spinal cord and the arm is interrupted, causing loss of function and sensation from the shoulder to the fingertips.
When Frank and former postdoctoral associate Pamela Harvey first tried to repair the brachial plexus in rodents, it produced mixed results: the researchers were able to stimulate new nerve growth, but the nerves did not re-grow to the proper positions in the spinal cord, and arm function was only partially restored.
Now, the pair has made what seems like a breakthrough. They found that when they applied a protein called artemin to the injured nerves, it caused significant growth and appears to have guided nerves back to their original sites in the spinal cord. Their research was published in June in PNAS: Proceedings of the National Academy of Sciences.
“In contrast to the haphazard growth we saw in our earlier stages of research, artemin treatments guide growing nerves back to their ‘home’ on the spinal cord, restoring near-normal use of the arm,” says Frank. “This is the first time we have seen this level of specificity in nerve regeneration within the central nervous system.”
Frank believes that these findings indicate that the mammalian spinal cord contains the cues needed to guide regenerating neurons to their connection sites. If this theory holds true, further study of artemin may lead to more generalized approaches to nerve regeneration.
“A possible explanation for this result is that artemin acts directly on the sensory cells themselves, rather than modifying the environment surrounding the growing nerve fibers within the spinal cord,” suggests Frank. “Other therapeutic agents that result in non-specific regeneration are applied directly to the spinal cord, and may therefore disrupt the cues needed for correct guidance.”
Frank and Harvey are hopeful that further study of artemin will lay the groundwork for treating humans.
“Not all nerves in the body are sensitive to artemin, but our approach may help other researchers find treatments that activate the spinal cord’s cues in the same way,” says Frank.
Lindsay Peterson, N10, received a master’s in nutrition communication from the Friedman School of Nutrition Science and Policy.
