The problem of axonal injury in the brains of veterans with histories of blast exposure
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  • 作者:Jiwon Ryu (1)
    Iren Horkayne-Szakaly (2)
    Leyan Xu (1)
    Olga Pletnikova (1)
    Francesco Leri (5)
    Charles Eberhart (1)
    Juan C Troncoso (1)
    Vassilis E Koliatsos (1) (3) (4)

    1. Department of Pathology
    ; Division of Neuropathology ; Johns Hopkins University School of Medicine ; Baltimore ; MD ; 21205 ; USA
    2. Department of Neuropathology & Ophthalmic Pathology
    ; Joint Pathology Center ; Defense Health Agency ; 606 Stephen Sitter Ave. ; Silver Spring ; MD ; 20910 ; USA
    5. Department of Psychology
    ; University of Guelph ; Guelph ; ON ; N1G 2聽W1 ; Canada
    3. Department of Neurology
    ; Johns Hopkins University School of Medicine ; Baltimore ; MD ; 21205 ; USA
    4. Department of Psychiatry and Behavioral Sciences
    ; Johns Hopkins University School of Medicine ; Baltimore ; MD ; 21205 ; USA
  • 关键词:Traumatic brain injury ; Diffuse axonal injury ; APP ; Axon bulbs ; Opiate ; Microglia
  • 刊名:Acta Neuropathologica Communications
  • 出版年:2014
  • 出版时间:December 2014
  • 年:2014
  • 卷:2
  • 期:1
  • 全文大小:2,290 KB
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  • 刊物主题:Neurosciences;
  • 出版者:BioMed Central
  • ISSN:2051-5960
文摘
Introduction Blast injury to brain, a hundred-year old problem with poorly characterized neuropathology, has resurfaced as health concern in recent deployments in Iraq and Afghanistan. To characterize the neuropathology of blast injury, we examined the brains of veterans for the presence of amyloid precursor protein (APP)-positive axonal swellings typical of diffuse axonal injury (DAI) and compared them to healthy controls as well as controls with opiate overdose, anoxic-ischemic encephalopathy, and non-blast TBI (falls and motor vehicle crashes). Results In cases with blast history, we found APP (+) axonal abnormalities in several brain sites, especially the medial dorsal frontal white matter. In white matter, these abnormalities were featured primarily by clusters of axonal spheroids or varicosities in a honeycomb pattern with perivascular distribution. Axonal abnormalities colocalized with IBA1 (+) reactive microglia and had an appearance that was distinct from classical DAI encountered in TBI due to motor vehicle crashes. Opiate overdose cases also showed APP (+) axonal abnormalities, but the intensity of these lesions was lower compared to cases with blast histories and there was no clear association of such lesions with microglial activation. Conclusions Our findings demonstrate that many cases with history of blast exposure are featured by APP (+) axonopathy that may be related to blast exposure, but an important role for opiate overdose, antemortem anoxia, and concurrent blunt TBI events in war theater or elsewhere cannot be discounted.

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