Study offers evidence into treating blast-associated TBI

Randy Rozek • October 26, 2016

A brain injury can directly alter many aspects of a person’s life, including their personality.

Andrew Pieper, University of Iowa Professor of psychiatry, recently led a new study in mice that has shown early damage to axons to be the key to the development of the subsequent long-term neurological complications that develop after blast injury, according to an article by Kasra Zarei in The Daily Iowan.

“Blast-associated injuries have become the signature injury for U.S. soldiers serving in the Middle East, creating a great need for targeted therapies,” the article reads. “‘Before

[the experiment] we knew that axons degenerated, but it was unknown whether this degeneration was a determinative critical step in blast-associated [injury] or a consequence of the broader picture of injury,’ Pieper said.”

Axonal damage being connected to blast-associated injuries is not a new concept, but its specific role as a driving force of damage has been unknown.

“Pieper and his team used an established model of mice that carry a genetic mutation and is resistant to some forms of axonal degeneration,” the article reads. ‘We had a model in place — we wanted to answer whether specifically blocking axonal injury would reduce the broad spectrum of functional deficits that normal mice experience after blast injury,’ Pieper said. The study showed that mice with axonal injury blocked do not develop the expected neurological deficits that genetically normal mice experience.”

Pieper’s team studied neurological deficits from multiple angles, including learning and memory, motor coordination and visual function. The mutant mice resistant to axonal degeneration maintained function in all categories, unlike the genetically normal mice, the article explains.

“The study demonstrated that axonal degeneration is a critical early event in blast-associated injury. Thus, therapies targeted at preventing or mitigating early axonal degeneration may provide a beneficial approach for treating those affected,” the article reads. “We have confirmation of the fact that axonal degeneration is crucial in this mechanism and driving neurobehavioral complications after blast-injury,” Pieper said. “Therefore, treatments aimed at preserving axons are worthwhile to further explore as possible new ways to treat patients suffering from this condition.”

The study also provides the potential opportunity to vet possible pharmacological treatments that may prove valuable for treating blast-associated brain injuries.

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