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Traumatic white matter injury and glial activation: From basic science to clinics

Authors

  • Zhifeng Kou,

    Corresponding author
    1. Department of Biomedical Engineering, Wayne State University, Detroit, Michigan
    2. Department of Radiology, Wayne State University, Detroit, Michigan
    • Address correspondence to Zhifeng Kou, Department of Biomedical Engineering, Wayne State University, Detroit, Michigan 48201, USA. E-mail: zhifeng_kou@wayne.edu or Pamela J. VandeVord, School of Biomedical Engineering and Sciences, Virginia Tech University, Blacksburg, Virginia 24061, USA. E-mail: pvord@vt.edu

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  • Pamela J. VandeVord

    Corresponding author
    1. School of Biomedical Engineering and Sciences, Virginia Tech University, Blacksburg, Virginia
    2. Salem VA Medical Center, Research & Development Service, Salem, Virginia
    • Address correspondence to Zhifeng Kou, Department of Biomedical Engineering, Wayne State University, Detroit, Michigan 48201, USA. E-mail: zhifeng_kou@wayne.edu or Pamela J. VandeVord, School of Biomedical Engineering and Sciences, Virginia Tech University, Blacksburg, Virginia 24061, USA. E-mail: pvord@vt.edu

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Abstract

An improved understanding and characterization of glial activation and its relationship with white matter injury will likely serve as a novel treatment target to curb post injury inflammation and promote axonal remyelination after brain trauma. Traumatic brain injury (TBI) is a significant public healthcare burden and a leading cause of death and disability in the United States. Particularly, traumatic white matter (WM) injury or traumatic axonal injury has been reported as being associated with patients' poor outcomes. However, there is very limited data reporting the importance of glial activation after TBI and its interaction with WM injury. This article presents a systematic review of traumatic WM injury and the associated glial activation, from basic science to clinical diagnosis and prognosis, from advanced neuroimaging perspective. It concludes that there is a disconnection between WM injury research and the essential role of glia which serve to restore a healthy environment for axonal regeneration following WM injury. Particularly, there is a significant lack of non-invasive means to characterize the complex pathophysiology of WM injury and glial activation in both animal models and in humans. An improved understanding and characterization of the relationship between glia and WM injury will likely serve as a novel treatment target to curb post injury inflammation and promote axonal remyelination. GLIA 2014;62:1831–1855

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