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Brain Injury Heals With Organ's Version of Pot?

Experiment shows natural brain chemical similar to marijuana may protect nerves

WEDNESDAY, Oct. 3, 2001 (HealthDayNews) -- A natural brain chemical that's similar to the active ingredient in marijuana may help heal brain injuries, say researchers.

The body's natural version of a cannabinoid, called 2-arachidonoyl glycerol (2-AG), reduced brain swelling, cell death and inflammation in mice with brain injuries, say scientists at Hebrew University in Jerusalem. Animals given 2-AG recovered more of their movement and mental sharpness than those that didn't get it, suggesting a drug made with the cannabinoid one day could be used to treat brain injuries in humans, the researchers say.

Some scientists have done research in the past that seems to show a protective effect -- at least in the test tube -- of THC, marijuana's active ingredient, in brain and nerve injury, says Esther Shohami, associate professor in pharmacology at Hebrew University where THC was first identified in the 1960s. She says because "THC mimics the activities of 2-AG," the researchers decided to use 2-AG in mice to see if it too would protect nerves.

Shohami says the researchers also have identified two natural chemicals -- endogenous cannabinoids -- in the human brain which may play a role in short-term memory, motor coordination, appetite and pain. The findings will appear in the Oct. 4 issue of the journal Nature.

"In a mouse model, we induced [brain] injury similar to those observed in patients. We treated the injured mice once, at one hour after injury, with 2-AG and found that the secondary damage, which is typical after the injury, is reduced," Shohami says. Less water pooled in the brain, there was better recovery of movement, fewer brain cells died and less of the brain was injured, she says.

2-AG may keep the brain from releasing toxic chemicals that cause cell damage and death after an injury, Shohami suggests. It also may improve blood circulation in the brain while slowing the release of chemicals that cause inflammation and cell death after injury. And what happens in a mouse brain also may happen in a human brain, Shohami says. "The basic mechanisms that are activated in the brain are similar between animal and human models."

Brain injury is the major cause of death in the young population in the Western world, Shohami says. "The processes in the brain after trauma that lead to death or injury are only partially understood. After the initial injury, the brain produces compounds which cause further damage, and, at the same time, produces other compounds that may be protective. Apparently the endocannabinoid system is part of this neuroprotective mechanism."

"From a practical point of view, a compound, which reduces the damage caused by brain trauma may be of significant importance in particular since no such drugs are available," Shohami says.

"Although 2-AG is a natural product produced in our brain, further research is needed before we introduce it into clinical use. However, I do believe it is a new avenue that should be pursued by the pharmaceutical industries." Shohami says.

"This is exciting news," says Stanley Thayer, professor of pharmacology at the University of Minnesota Medical School in Minneapolis. "This research highlights how little we know about this endocannabinoid system. What we have here is a dramatic example of how this system may be involved in a response to a traumatic head injury."

"Our treatment of brain injury is very limited. We don't have much we can do to treat trauma, stroke or neurodegenerative disease. So this study shows some potential because it also identifies several potential targets for drug therapies -- not only the brain receptors where the psychoactive ingredient in marijuana, THC, operates. The other targets could be the processes that synthesize and metabolize these molecules like 2-AG."

"Those could be more subtle targets, with fewer side effects," Thayer says.

What To Do: For more on cannabinoids and the brain, see the Society for Neuroscience or the Brain Injury Association of America.

SOURCES: Interviews with Esther Shohami, Ph.D., associate professor, pharmacology, Hebrew University, Jerusalem, Israel, and Stanley Thayer, Ph.D., professor of pharmacology, University of Minnesota Medical School, Minneapolis; Oct. 4, 2001, Nature
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