73
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      What’s New in Traumatic Brain Injury: Update on Tracking, Monitoring and Treatment

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Traumatic brain injury (TBI), defined as an alteration in brain functions caused by an external force, is responsible for high morbidity and mortality around the world. It is important to identify and treat TBI victims as early as possible. Tracking and monitoring TBI with neuroimaging technologies, including functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET), and high definition fiber tracking (HDFT) show increasing sensitivity and specificity. Classical electrophysiological monitoring, together with newly established brain-on-chip, cerebral microdialysis techniques, both benefit TBI. First generation molecular biomarkers, based on genomic and proteomic changes following TBI, have proven effective and economical. It is conceivable that TBI-specific biomarkers will be developed with the combination of systems biology and bioinformation strategies. Advances in treatment of TBI include stem cell-based and nanotechnology-based therapy, physical and pharmaceutical interventions and also new use in TBI for approved drugs which all present favorable promise in preventing and reversing TBI.

          Related collections

          Most cited references370

          • Record: found
          • Abstract: not found
          • Article: not found

          Glutamate neurotoxicity and diseases of the nervous system.

          D Choi (1988)
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention.

            Traumatic brain injury (TBI) remains one of the leading causes of mortality and morbidity worldwide, yet despite extensive efforts to develop neuroprotective therapies for this devastating disorder there have been no successful outcomes in human clinical trials to date. Following the primary mechanical insult TBI results in delayed secondary injury events due to neurochemical, metabolic and cellular changes that account for many of the neurological deficits observed after TBI. The development of secondary injury represents a window of opportunity for therapeutic intervention to prevent progressive tissue damage and loss of function after injury. To establish effective neuroprotective treatments for TBI it is essential to fully understand the complex cellular and molecular events that contribute to secondary injury. Neuroinflammation is well established as a key secondary injury mechanism after TBI, and it has been long considered to contribute to the damage sustained following brain injury. However, experimental and clinical research indicates that neuroinflammation after TBI can have both detrimental and beneficial effects, and these likely differ in the acute and delayed phases after injury. The key to developing future anti-inflammatory based neuroprotective treatments for TBI is to minimize the detrimental and neurotoxic effects of neuroinflammation while promoting the beneficial and neurotrophic effects, thereby creating optimal conditions for regeneration and repair after injury. This review outlines how post-traumatic neuroinflammation contributes to secondary injury after TBI, and discusses the complex and varied responses of the primary innate immune cells of the brain, microglia, to injury. In addition, emerging experimental anti-inflammatory and multipotential drug treatment strategies for TBI are discussed, as well as some of the challenges faced by the research community to translate promising neuroprotective drug treatments to the clinic. Copyright © 2012 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              BACE1 is the major beta-secretase for generation of Abeta peptides by neurons.

                Bookmark

                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Int J Mol Sci
                Int J Mol Sci
                ijms
                International Journal of Molecular Sciences
                MDPI
                1422-0067
                26 May 2015
                June 2015
                : 16
                : 6
                : 11903-11965
                Affiliations
                [1 ]Department of Anesthesiology, Loma Linda University Medical Center, Loma Linda, CA 92354, USA; E-Mails: cesarreis@ 123456hotmail.com (C.R.); rapplegate@ 123456llu.edu (R.A.); gstier@ 123456llu.edu (G.S.); rdmartin@ 123456llu.edu (R.M.)
                [2 ]Department of Physiology and Pharmacology, Loma Linda University School of Medicine, 11041 Campus Street, Risley Hall, Room 219, Loma Linda, CA 92354, USA; E-Mails: monkeymei2@ 123456aliyun.com (Y.W.); onatakyol@ 123456hotmail.com (O.A.); wingiho@ 123456googlemail.com (W.M.H.)
                [3 ]Department of Physiology, School of Medicine, University of Jinan, Guangzhou 250012, China
                [4 ]Department of Neurosurgery, University Hospital Innsbruck, Tyrol 6020, Austria
                [5 ]Department of Neurosurgery, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA
                Author notes
                [†]

                These authors contributed equally to this work.

                [* ]Author to whom correspondence should be addressed; E-Mail: johnzhang3910@ 123456yahoo.com ; Tel.: +1-909-558-4723.
                Article
                ijms-16-11903
                10.3390/ijms160611903
                4490422
                26016501
                de8be3b1-7618-445a-aa12-910e32829e1a
                © 2015 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 26 March 2015
                : 06 May 2015
                Categories
                Review

                Molecular biology
                traumatic brain injury,neuroimaging,electrophysiology,stem cell,hypothermia,nano particle,biomarker,microdialysis,proteomic,genomic

                Comments

                Comment on this article