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      Chronic Repetitive Mild Traumatic Brain Injury Results in Reduced Cerebral Blood Flow, Axonal Injury, Gliosis, and Increased T-Tau and Tau Oligomers

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          Abstract

          Exposure to repetitive mild traumatic brain injury (mTBI) is a risk factor for chronic traumatic encephalopathy, which is characterized by patchy deposition of hyperphosphorylated tau aggregates in neurons and astrocytes at the depths of cortical sulci. We developed an mTBI paradigm to explore effects of repetitive concussive-type injury over several months in mice with a human tau genetic background (hTau). Two injuries were induced in the hTau mice weekly over a period of 3 or 4 months and the effects were compared with those in noninjured sham animals. Behavioral and in vivo measures and detailed neuropathological assessments were conducted 6 months after the first injury. Our data confirm impairment in cerebral blood flow and white matter damage. This was accompanied by a 2-fold increase in total tau levels and mild increases in tau oligomers/conformers and pTau (Thr231) species in brain gray matter. There was no evidence of neurofibrillary/astroglial tangles, neuropil threads, or perivascular foci of tau immunoreactivity. There were neurobehavioral deficits (ie, disinhibition and impaired cognitive performance) in the mTBI animals. These data support the relevance of this new mTBI injury model for studying the consequences of chronic repetitive mTBI in humans, and the role of tau in TBI.

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          Author and article information

          Journal
          J Neuropathol Exp Neurol
          J. Neuropathol. Exp. Neurol
          jnen
          jnen
          Journal of Neuropathology and Experimental Neurology
          Oxford University Press
          0022-3069
          1554-6578
          July 2016
          31 May 2016
          : 75
          : 7
          : 636-655
          Affiliations
          From the Roskamp Institute, Sarasota, Florida (JOO, BM, MA, PL, CL, LA, JE, MM, CB, FC); James A. Haley Veterans’ Hospital, Tampa, Florida (BM, LA, CB, FC); Open University, Milton Keynes, UK (BM, MA, CL, CB, FC); Bay Pines VA Healthcare System, Bay Pines, Florida (CB); Queen Elizabeth University Hospital, Glasgow, UK (WS); University of Glasgow, Glasgow, UK (WS); and University of Pennsylvania, Philadelphia, Pennsylvania (WS).
          Author notes

          This study was funded by the Roskamp Foundation.

          The authors have no duality or conflicts of interest to declare.

          Send correspondence to: Joseph O. Ojo, PhD, Neuropathology Core Unit, Roskamp Institute, 2040 Whitfield Ave., Sarasota, FL 34324; E-mail: bojo@ 123456roskampinstitute.net
          Article
          PMC4913432 PMC4913432 4913432 nlw035
          10.1093/jnen/nlw035
          4913432
          27251042
          90900b6a-d804-4b42-a1af-cc0eb57b60cb
          © 2016 American Association of Neuropathologists, Inc. All rights reserved.
          Page count
          Pages: 20
          Categories
          Original Articles

          Cerebral blood flow,Concussion,Glial activation,hTau mice,Tau.,Axonal injury,Behavior

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