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Science Translational Medicine: Blast-Related Injuries May Increase Veterans’ Risk of Brain Disorder

Military veterans that have suffered a blast-related brain injury may be at increased risk for developing chronic traumatic encephalopathy or CTE, a degenerative brain disease also found in people such as hockey players and American football players with a history of repetitive brain trauma.

The research appears in the 16 May issue of the journal Science Translational Medicine.

CTE is marked by progressive brain tissue degeneration and build-up of abnormal tau protein, which leads to chunks of neurofibrillary tangles in the brain, as seen in Alzheimer’s patients. Its symptoms include memory problems, suicidal thoughts, aggression, and dementia. Patients can develop CTE many years after brain trauma, and the disease is often seen in athletes who have suffered from repeated concussions.

Soldiers and civilians in combat zones are at risk for developing traumatic brain injury (TBI) caused by blast explosions from improvised explosive devices. Traumatic brain injury may affect 20% of the 2.3 million servicemen and women deployed since 2001. Yet the long-term effects of blast exposure remain murky.

“Our study provides compelling evidence that blast TBI and CTE are structural brain disorders that can emerge as a result of brain injury on the battlefield or playing field,” said Lee Goldstein, an associate professor at Boston University School of Medicine and lead author of the study.

In their analysis of brain tissue from eight deceased military veterans and athletes, Goldstein and colleagues found evidence of CTE such as tau protein build-up and progressive neurodegeneration. While many of the athletes had suffered from multiple head concussions, most of the veterans in the study experienced only one or two blast-related incidents.

The team next created a mouse model of blast exposure by developing a special blast shock tube to deliver traumatic brain injury to mice. Injured mouse brain tissue shared many CTE characteristics with the diseased human brain tissue, and just one blast was sufficient to cause CTE in the animals.

The mice also had learning and memory problems, but mice whose heads were held still during brain injury had noticeably less difficulty with mental tasks after the blast. The findings hint that blast-related traumatic brain injury and CTE may come from head acceleration due to blast wind, the rapid movement of air caused by an explosion.

“The blast wind from an IED can reach a velocity of up to 330 miles per hour, which is greater than the largest wind gust ever recorded on earth,” Goldstein said. “The force of the blast wind causes the head to move so forcefully that it can result in damage to the brain.”


Read the abstract, “Chronic Traumatic Encephalopathy in Blast-Exposed Military Veterans and a Blast Neurotrauma Mouse Model,” by L.E. Goldstein and colleagues.


Nadia Ramlagan

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