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Investigators from Boston University (BU) and the Veterans AffairsBoston Healthcare System have shown evidence of chronic traumaticencephalopathy (CTE) in brain tissue from blast-exposed militaryservice personnel. Laboratory experiments conducted by theinvestigators demonstrated that exposure to a single blastequivalent to a typical improvised explosive device (IED) resultsin CTE and long-term brain impairments that accompany the disease.They also found that the blast wind, not the shock wave, from theIED blast leads to traumatic brain injury (TBI) and long-term consequences, including CTE. This research, which represents the first case series of postmortembrains from U.S. military personnel who were exposed to a blastand/or a concussive injury, wase published online by Science Translational Medicine. Lee Goldstein, MD, PhD, associate professor at Boston UniversitySchool of Medicine (BUSM) and Boston University College ofEngineering, and Ann McKee, MD, professor at BUSM and director ofthe Neuropathology Service for VA New England Healthcare System,led this international collaborative study and are the seniorco-authors. CTE, which can only be diagnosed postmortem, is a progressiveneurodegenerative brain disorder that has been reported in athleteswith multiple concussions or subconcussive injuries. In early stages, CTE is characterizedby the presence of abnormal deposits of a protein called tau in theform of neurofibrillary tangles, glial tangles and neuropil threadsthroughout the brain. These tau lesions eventually lead to braincell death. CTE has clinical features in common with TBI, includingpsychiatric symptoms and long-term cognitive disability involvingmemory and learning deficits. TBI can impact military personnelexposed to an explosive blast and may affect approximately 20percent of the 2.3 million servicemen and women deployed since2001. In this study, investigators performed comprehensiveneuropathological analyses on brain tissue from four militaryservice personnel with known blast exposure and/or concussiveinjury. They compared these results with brain tissue samples fromthree young amateur American football players and a professionalwrestler, all of whom had a history of repetitive concussiveinjury, and four samples from comparably-aged normal controls withno history of blast exposure, concussive injury or neurologicaldisease. The investigators found that CTE neuropathology in the brains ofblast-exposed military veterans was similar to that found in youngathletes with repetitive concussion and consistent with what haspreviously been observed in brain samples from other athletes witha history of repetitive concussive injury. "Our results showed that the neuropathology from blast exposure,concussive injury, or both were virtually indistinguishable fromthose with a history of repeat concussive injury," said McKee, whois the director of the Brain Banks for BU's Alzheimer's DiseaseCenter and the Center for the Study of Traumatic Encephalopathy,which are based at the Bedford VA Medical Center. McKee said thatthese findings indicate that TBI caused by different factors maytrigger similar disease pathways in the brain. "The neuropsychiatric symptoms of CTE that have previously beenassociated with athletes diagnosed with CTE could also beattributed to military personnel who were exposed to blast," saidGoldstein, who also is affiliated with the BU Photonics Center andserved as the study's lead author. To examine the impact of a single blast exposure, the investigatorscollaborated with leading experts in blast physics, experimentalpathology and neurophysiology at Boston University, VA BostonHealthcare System, White River Junction VA Medical Center, New YorkMedical College, Fraunhofer Center for Manufacturing Innovation,University of Massachusetts Lowell, Lawrence Livermore NationalLaboratory, Massachusetts General Hospital and the University ofOxford. The team's experimental data showed that one blastcomparable to that experienced by military service personnel in thefield resulted in both neuropathological and behavioral evidence ofCTE. Surprisingly, the long-term impairments in brain function,including impaired learning and memory, were observed just twoweeks after exposure to a single blast. The blast wind from an IED can reach a velocity of up to 330 milesper hour, which is greater than the largest wind gust ever recordedon earth. "The force of the blast wind causes the head to move soforcefully that it can result in damage to the brain," saidGoldstein. Based on the results, the investigators went a step further andexplored how they could prevent the brain injury. They demonstratedthat immobilizing the head during a blast exposure prevented thelearning and memory deficits associated with CTE that occurred whenthe head was not immobilized. "Our study provides compelling evidence that blast TBI and CTE arestructural brain disorders that can emerge as a result of braininjury on the battlefield or playing field," added Goldstein. "Nowthat we have identified the mechanism responsible for CTE, we canwork on developing ways to prevent it so that we can protectathletes and our military service personnel." The study results provide a pathway for the development of noveldiagnostic strategies for blast-related brain trauma, as well as totreat and rehabilitate those who have been exposed to blast and/ora concussive injury. 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