Enzyme May Clear Path for Nerve Growth in Injured Spine

Study in rats points to potential human therapy

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By
HealthDay Reporter

WEDNESDAY, April 10, 2002 (HealthDayNews) -- A bacterial enzyme that clears a path for nerve regeneration could someday be used in therapies for people with partial or complete spinal cord injuries.

A study by British researchers reports that rats with partial spinal cord injuries regained neurological function and their ability to walk normally after treatment with the enzyme, known as chondroitinase ABC (ChABC).

Their findings appear in tomorrow's issue of Nature.

While previous research had shown this enzyme could make nerve fibers regenerate in the brain, co-author Dr. James W. Fawcett, a professor at the University of Cambridge's Centre for Brain Repair, says this study is the first demonstration of the enzyme's effect on the spinal cord.

In the study, the researchers simulated a crushing spinal cord injury, affecting most of the sensory portion of the spinal cord and part of the motor pathway. The damage stopped short of causing paralysis, but the partial injury left the animals unable to walk well.

The researchers then compared the effect of treating the rats with ChABC versus a placebo.

Unlike the placebo-treated animals, the sensory neurons in the ChABC-treated rats grew up to 4 millimeters towards the brain, while motor neurons regenerated downwards from the site of the injury. The team also measured a return of electrical signaling between the brain's cerebral cortex and the spinal cord, although the signal was slower and weaker.

Most exciting of all, the ChABC-treated rats showed significant recovery of neurological function, returning to a normal walking gait. However, their senses and motor function were not fully restored. In comparison, the placebo-treated animals show little neurological recovery after their injuries.

Fawcett says while he anticipates this therapy would have the same effect in complete spinal cord injuries, it may work best in partial injuries. He says two-thirds of human spinal cord injuries are partial.

The bacterial ChABC targets chondroitin sulphate proteogylcan (CSPG) molecules, which are among the body's standard injury defenses. Fawcett says they may normally function to keep bacteria out and prevent infection. "This is the reason, probably, why bacteria have invented an enzyme to digest it, to make it easier for them to get into injuries," he says.

In an accompanying commentary, neuroscience professor Lars Olson of Sweden's Karolinska Institute compares the use of ChABC to pruning shrubbery in the path of the nerve fibers. "It's a very significant finding," he says.

However, both Olson and the researchers stress human therapies for treating spinal cord injuries will have to target multiple obstacles. First, treatment strategies will need to provide a "bridge" between two nerve stumps, upon which new nerve growth can occur.

At the same time, therapies such as ChABC will need to clear a path for growth. Finally, other compounds will have to stimulate nerve growth and neutralize any factors that interfere with the regenerative progress.

Olson suspects clinical trials of this therapy could start in humans within five years, an estimate echoed by the International Spinal Research Trust fund.

Fawcett says the findings could lead to therapies that improve the quality of life for people with spinal cord injuries.

"Our main target for people with spinal cord injuries is not to completely repair their spinal cord, because we don't think that's possible with present technology," Fawcett says.

Instead, he says, this could lead to small repairs that may restore hand function or even allow a paralyzed person dependent on a respirator to breathe on his own.

What To Do: Check out this spinal cord tutorial from the Christopher Reeve Paralysis Foundation. You can also visit SpinalInjury.Net or the National Institute of Neurological Disorders and Stroke to find out more about spinal cord injuries.

SOURCES: James W. Fawcett, M.D., Ph.D., professor, Department of Physiology, Centre for Brain Repair, University of Cambridge, Cambridge, England; Lars Olson, Ph.D., professor, Department of Neuroscience, Karolinska Institute, Stockholm, Sweden; April 11, 2002, Nature

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