Blue dye shuts down spinal cord injuries

U. ROCHESTER (US)—A common food additive that gives M&Ms and Gatorade their blue tint may offer promise for preventing the additional—and serious—secondary damage that immediately follows a traumatic injury to the spinal cord.

In an article published online July 28 in the Proceedings of the National Academy of Sciences, researchers at the University of Rochester Medical Center report that the compound Brilliant Blue G (BBG) stops the cascade of molecular events that cause secondary damage to the spinal cord in the hours following a spinal injury.

A research team led by Maiken Nedergaard, professor of neurosurgery and director of the Center for Translational Neuromedicine, discovered that BBG is both structurally and functionally equivalent to the commonly used FD&C blue dye No. 1, which has been approved by the Food and Drug Administration since 1982.

“Because BBG is so similar to this commonly used blue food dye, we felt that if it had the same potency in stopping the secondary injury as oxidized ATP, but with none of its side effects, then it might be great potential treatment for cord injury,” Nedergaard explains.

The team’s hunch paid off. An intravenous injection of BBG proved to significantly reduce secondary injury in spinal cord-injured rats, which improved to the point of being able to walk, though with a limp. Rats that had not received the BBG solution never regained the ability to walk.

The new findings follow research from Rochester five years ago, which detailed how ATP, the energy source that keeps the body’s cells alive, quickly pour into the area surrounding a spinal cord injury shortly after it occurs, and paradoxically kills off what are otherwise healthy and uninjured cells.

That surprising discovery marked a milestone in establishing how secondary injury occurs in spinal cord patients and laid out a potential way to stop secondary spinal injury, by using oxidized ATP, a compound known to block ATP’s effects. Rats with damaged spinal cords who received an injection of oxidized ATP were shown to recover much of their limb function, to the point of being able to walk again, ambulating effectively if not gracefully.

“While we achieved great results when oxidized ATP was injected directly into the spinal cord, this method would not be practical for use with spinal cord-injured patients,” Nedergaard says.

“First, no one wants to put a needle into a spinal cord that has just been severely injured, so we knew we needed to find another way to quickly deliver an agent that would stop ATP from killing healthy motor neurons. Second, the compound we initially used, oxidized ATP, cannot be injected into the bloodstream because of its dangerous side effects.”

Nedergaard cautions that while the research offers a promising new way of treating spinal cord injury, it is still years away from possible application in patients.

In addition, any potential treatments would only be helpful to people who have just suffered a spinal cord injury, not for patients whose injury is more than a day old. Just as clot-busting agents can help patients who get to an emergency room within a few hours of having a stroke or heart attack, so a compound that could stem the damage from ATP might help patients who have had a spinal cord injury and are treated immediately.

“We have no effective treatment now for patients who have an acute spinal cord injury,” says Steven Goldman, chairman of the department of neurology.

“Our hope is that this work will lead to a practical, safe agent that can be given to patients shortly after injury, for the purpose of decreasing the secondary damage that we have to otherwise expect.”

The research was supported by the New York State Spinal Cord Injury program, the Miriam and Sheldon Adelson Medical Research Foundation, and grants from the National Institutes of Health.

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