Spinal Cord Research Shows Promise

Researchers at Montreal Neurological Institute say they have identified a protein that could be manipulated to make spinal cord injuries repair themselves.

Montreal researchers have identified what may be a pivotal first step toward regenerating injured spinal cords using the body’s own stem cells.

The repair mechanism that works well in a developing or embryonic nervous system seems to work in reverse in adults following injury, explained neuroscientist Tim Kennedy of the Montreal Neurological Institute.

That mechanism involves a protein called Netrin-1 that acts like a guidance cue for directing embryonic cells and helping the arm-like extension of cells, called the axon, grow in the right direction.

“This protein is essential for normal brain development, without it, no neural connections are made,” he explained, but its function in adults remains obscure.

Scientists have known for years that stem cells are present in the spinal cord but don’t pony up to replenish nerve cells so the body can repair itself.

The study identified Netrin-1 as the key molecule responsible for driving adult stem cells away from lesions and injuries in the spinal cord.

Published in Proceedings of the National Academy of Science this week with co-lead investigator Philip Horner of the University of Washington, the study suggests the Netrin-1 signal of attract-and-repel can be manipulated, opening the door to new therapies.

When Netrin-1 is blocked, adult stem cells stay at the injury site, Kennedy said.

There’s been a lot of excitement about adult stem cells because of their capacity to renew themselves after injury, Kennedy said.

“What’s known is that they exist and that they have the capacity to form all sorts of cells in the nervous system,” he said.

“What we’re seeing here is a way to direct them to specific places.”

Although done in vitro, scientists are far from showing successful therapy in animal models.

By: Charlie Fidelman

Posted on November 16th, 2007 in Research for a Cure. Tagged: