More MS news articles for May 2002

Protein helps rats' nerves regrow after injury

http://my.webmd.com/content/article/3053.1491?z=1728_00000_1000_ln_07

2002-05-29 13:50:26 -0400
By Merritt McKinney
Reuters Health
NEW YORK

Scientists have identified a protein bit that promotes the regrowth of nerve fibers after a spinal cord injury.

The encouraging results come from a rat study, but they could point the way to the development of a drug to reverse damage from spinal cord injury, brain injury or some kinds of stroke and multiple sclerosis, according to the study's authors.

Dr. Stephen M. Strittmatter of Yale University in New Haven, Connecticut, told Reuters Health that there is an inhibitor called Nogo in the brain and spinal cord that keeps nerve fibers from growing back after an injury. This lack of nerve fiber growth is the reason why many people become paralyzed after a brain or spinal cord injury, he explained.

In the study in rats, Strittmatter and his colleagues discovered a peptide compound, NEP1-40, which blocks the effects of Nogo by binding to its receptor in the brain. When the researchers delivered the peptide directly into the spinal cords of injured rats, the rodents recovered some of their ability to walk.

Compared with injured rats that were not given NEP1-40, the treated rats were still better off nearly a month later, according to the report published in the May 30th issue of the journal Nature.

"A therapeutic agent with similar action might be developed for humans that would promote nerve fiber growth after spinal cord injury, head trauma or stroke," Strittmatter said.

Researchers have a long way to go before any such drug can be tested in humans, however, according to the Yale researcher. The Nogo blocker needs to be refined and studied to make sure that it does not cause harmful side effects, he said. The goal is to maximize the compound's potency, effectiveness and stability, he added.

The best time to give the Nogo blocker after an injury is uncertain, Strittmatter noted. He explained that in the rat study, NEP1-40 was given over the course of 4 weeks, but treatment began right after the injury. It remains unclear, he said, whether the compound could be given later and still be effective.

Once the best version of the Nogo receptor blocker is developed, it should be tested in animals with other sorts of injuries, according to Strittmatter.

"This will ensure that only the safest compound with a high chance for efficacy is administered to humans," he said.

The study was funded in part by Biogen Inc.

SOURCE: Nature 2002;417:547-551.
 

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