@article{ref1,
title="Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model",
journal="Science translational medicine",
year="2012",
author="Goldstein, Lee E. and Fisher, Andrew M. and Tagge, Chad A. and Zhang, Xiao-Lei and Velisek, Libor and Sullivan, John A. and Upreti, Chirag and Kracht, Jonathan M. and Ericsson, Maria and Wojnarowicz, Mark W. and Goletiani, Cezar J. and Maglakelidze, Giorgi M. and Casey, Noel and Moncaster, Juliet A. and Minaeva, Olga and Moir, Robert D. and Nowinski, Christopher J. and Stern, Robert A. and Cantu, Robert C. and Geiling, James and Blusztajn, Jan K. and Wolozin, Benjamin L. and Ikezu, Tsuneya and Stein, Thor D. and Budson, Andrew E. and Kowall, Neil W. and Chargin, David and Sharon, Andre and Saman, Sudad and Hall, Garth F. and Moss, William C. and Cleveland, Robin O. and Tanzi, Rudolph E. and Stanton, Patric K. and McKee, Ann C.",
volume="4",
number="134",
pages="134ra60-134ra60",
abstract="Blast exposure is associated with traumatic brain injury (TBI), neuropsychiatric symptoms, and long-term cognitive disability. We examined a case series of postmortem brains from U.S. military veterans exposed to blast and/or concussive injury. We found evidence of chronic traumatic encephalopathy (CTE), a tau protein-linked neurodegenerative disease, that was similar to the CTE neuropathology observed in young amateur American football players and a professional wrestler with histories of concussive injuries. We developed a blast neurotrauma mouse model that recapitulated CTE-linked neuropathology in wild-type C57BL/6 mice 2 weeks after exposure to a single blast. Blast-exposed mice demonstrated phosphorylated tauopathy, myelinated axonopathy, microvasculopathy, chronic neuroinflammation, and neurodegeneration in the absence of macroscopic tissue damage or hemorrhage. Blast exposure induced persistent hippocampal-dependent learning and memory deficits that persisted for at least 1 month and correlated with impaired axonal conduction and defective activity-dependent long-term potentiation of synaptic transmission. Intracerebral pressure recordings demonstrated that shock waves traversed the mouse brain with minimal change and without thoracic contributions. Kinematic analysis revealed blast-induced head oscillation at accelerations sufficient to cause brain injury. Head immobilization during blast exposure prevented blast-induced learning and memory deficits. The contribution of blast wind to injurious head acceleration may be a primary injury mechanism leading to blast-related TBI and CTE. These results identify common pathogenic determinants leading to CTE in blast-exposed military veterans and head-injured athletes and additionally provide mechanistic evidence linking blast exposure to persistent impairments in neurophysiological function, learning, and memory.<p /> <p>Language: en</p>",
language="en",
issn="1946-6234",
doi="10.1126/scitranslmed.3003716",
url="http://dx.doi.org/10.1126/scitranslmed.3003716"
}