Scientists at Emory University School of Medicine were able to enhance significantly the re-growth of damaged peripheral nerves in mice by treating them with enzymes that counteracted a growth-blocking mechanism. The research offers the potential for improving functional recovery after peripheral nerve injuries. The Emory scientists were led by Arthur English, PhD, professor of cell biology, with faculty colleagues Robert McKeon, PhD and Erica Werner, PhD and former Emory student M.L. Groves. Results of the research will be presented at the annual meeting of the Society for Neuroscience on November 8 in New Orleans.

Peripheral nerves extend from the spinal cord to targets in the periphery such as muscle and skin. Individual peripheral nerves contain thousands of individual fibers, called axons, which project to specific targets. When a peripheral nerve is damaged, axons between the injury site and muscle or skin degenerate and function is lost. Although peripheral nerve axons are capable of regenerating after such injuries, in humans this regeneration is modest at best and there currently is no effective clinical treatment.

One reason peripheral nerves do not regenerate well is the presence of growth inhibitory substances, called proteoglycans, within the environment of the damaged nerve. In an effort to improve the ability of axons to regenerate, the Emory scientists attempted to modify this inhibitory environment following peripheral nerve injury in mice. They treated the peripheral portion of severed nerves with each of three enzymes that degrade specific types of proteoglycans.

During the first two weeks after the injury, axons regenerated through enzyme-treated tissues much more effectively than through untreated tissues. Not only did the axons regenerate, those that did extended more than twice as far.

"This study shows that treatment with enzymes that degrade proteoglycans offers the potential to enhance regenerat
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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University Health Sciences Center
8-Nov-2003

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