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Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model

: Goldstein, L.E.; Fisher, A.M.; Tagge, C.A.; Zhang, X.-L.; Velisek, L.; Sullivan, J.A.; Upreti, C.; Kracht, J.M.; Ericsson, M.; Wojnarowicz, M.W.; Goletiani, C.J.; Maglakelidze, G.M.; Casey, N.; Moncaster, J.A.; Minaeva, O.; Moir, R.D.; Nowinski, C.J.; Stern, R.A.; Cantu, R.C.; Geiling, J.; Blusztajn, J.K.; Wolozin, B.L.; Ikezu, T.; Stein, T.D.; Budson, A.E.; Kowall, N.W.; Chargin, D.; Sharon, A.; Saman, S.; Hall, G.F.; Moss, W.C.; Cleveland, R.O.; Tanzi, R.E.; Stanton, P.K.; McKee, A.C.


Science Translational Medicine 4 (2012), No.134, Art. 134ra60
ISSN: 1946-6234
Journal Article
Fraunhofer IPT ()

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 fo r 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 shockwaves 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 andmemory 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.