After years of work, a team of Harvard-affiliated researchers is one step closer to finding a possible treatment for stroke damage and spinal cord injuries.
According to head researcher Larry I. Benowitz, Harvard Medical School associate professor of neurosurgery, this discovery could have a huge impact in the long run.
"At the practical level, we hope it's going to help improve functional outcome after a stroke or spinal injury," he said.
Inosine, a molecule that appears naturally in small quantities in the human body, has been found in laboratory test rats to help reestablish connections after nervous system damage.
Three years ago, Benowitz said, his team of researchers found a very effective way to stimulate injured nerve cells to regenerate axons (nerve fibers) using inosine, but the uses and extent of that discovery were unclear. Now he and his colleagues have come closer to understanding how this molecule works.
Just this week in the Journal of Neuroscience, Benowitz published the new evidence his team had found.
After the body suffers a stroke or spinal cord injury, the central nervous system is unable to reestablish its connections through the nerve cells, therefore causing severe and often permanent loss of mobility.
By activating an enzyme that is used in transmitting signals within nerve cells, which Benowitz referred to as the "master switch," inosine stimulates the remaining nerve cells to express genes that enable them to extend a new axon.
Inosine is structurally similar to some of the molecules that make up DNA.
"Inosine passes through cell membranes, so it doesn't act on receptors," he said. "It gets right to the heart of the matter."
The benefits, especially in stroke victims, would be two-fold, Benowitz said, according to his laboratory research. A major problem with strokes is that not only are cells damaged, but also, cells that are not immediately killed lose their connections and die out over time.
Inosine can minimize the amount of damage to individual cells, while at the same time stimulating the nerve cells that are not damaged to re-establish new circuitry to replace lost connections.