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Blast simulation reveals how explosions hurt the brain

Blast simulation reveals how explosions hurt the brain

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Using rat neurons and human blood vessels, scientists create traumatic-brain-injury on a chip. Experiments identified the biochemical pathway involved, offering treatment hopes for veterans.

Harvard bioengineers have figured out the mechanics behind bomb-blast brain injuries.

More than 300,000 US troops have suffered a traumatic brain injury (TBI) in the current wars in Iraq and Afghanistan, and these findings offer new hopes for treating veterans wounded by explosive devices and grenades.

When delicate brain tissue slams against the skull, the results range from a temporary concussion to hemorrhaging to early onset of Alzheimer’s.

This month, two studies explain how those mechanical forces translate into subtly detrimental physiological changes in the brain.

After the initial impact, (1) the connections between nerve cells in the brain retract and (2) sometimes the blood vessels constrict (called vasospasm), Nature News explains. The new work shows that a signaling pathway – the Rho–ROCK pathway – is responsible for both of these effects.

"So many young men and women are returning from military service with brain injuries, and we just don't know how to help them,” says lead researcher, Harvard’s Kevin Kit Parker, a major in the US Army who served in Afghanistan.

He adds: “I kept seeing buddies of mine get hit and thought, ‘All right, I'll take a look at this and see if I can get an angle on it.’”

So, his team created a blast simulator device that abruptly stretches (1) cultured rat neurons and (2) engineered human blood vessel tissue in ways that mimic blast waves traveling through the brain.

After a series of biochemical experiments, they found:

  • The mechanical force disrupted proteins called integrins that help anchor cells to the scaffold of protein that surrounds them, ScienceNOW explains.
  • Likely, the rapid stretching of blood vessels or neurons ‘plucks’ the integrins with more force than they’re designed to handle – overstimulating the Rho-ROCK pathway, causing neuronal extensions (or axons) to withdraw and blood vessels to constrict.
  • When the researchers applied a Rho–ROCK pathway inhibitor, injury to neurons and blood vessel tissue was either delayed or prevented.

Because the same pathway is involved in both blood vessels and neurons, one drug could address both problems. But these culture dish findings need to be tested on animals and humans: “It would be inappropriate to extrapolate from a dish to some dude's head," Parker says.

Also, this ‘TBI on a chip’ could one day be used to screen for drugs to treat blast-injured soldiers before long-term damage sets in.

Their work was published in the Proceedings of the National Academy of Sciences and PLoS ONE this month.

Via Nature News, ScienceNOW.

Subject matter too heavy? Last month, neurosurgeons examined 704 head injuries in the Asterix comic books and concluded that “no permanent deficit could be found.”

Image by The U.S. Army via Flickr

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Janet Fang

Contributing Editor

Janet Fang has written for Nature, Discover and the Point Reyes Light. She is currently a lab technician at Lamont-Doherty Earth Observatory. She holds degrees from the University of California, Berkeley and Columbia University. She is based in New York. Follow her on Twitter. Disclosure