Neuroprotective Strategies for Traumatic Brain Injury: Improving Clinical Translation
by
Shruti V. Kabadi and Alan I. Faden *
Shruti V. Kabadi and Alan I. Faden *
Department of Anesthesiology, Center for Shock, Trauma and Anesthesiology Research (STAR), National Study Center for Trauma and EMS, University of Maryland School of Medicine, Baltimore, MD 21201, USA
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2014, 15(1), 1216-1236; https://doi.org/10.3390/ijms15011216
Received: 11 December 2013 / Revised: 7 January 2014 / Accepted: 13 January 2014 / Published: 17 January 2014
(This article belongs to the Special Issue Neuroprotective Strategies 2014)
Traumatic brain injury (TBI) induces secondary biochemical changes that contribute to delayed neuroinflammation, neuronal cell death, and neurological dysfunction. Attenuating such secondary injury has provided the conceptual basis for neuroprotective treatments. Despite strong experimental data, more than 30 clinical trials of neuroprotection in TBI patients have failed. In part, these failures likely reflect methodological differences between the clinical and animal studies, as well as inadequate pre-clinical evaluation and/or trial design problems. However, recent changes in experimental approach and advances in clinical trial methodology have raised the potential for successful clinical translation. Here we critically analyze the current limitations and translational opportunities for developing successful neuroprotective therapies for TBI.
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Keywords:
experimental head injury; clinical trial design; translational challenges; multipotential neuroprotective approaches; programmed cell death; caspase-dependent and AIF-mediated cell death; microglial and astrocyte activation; autophagy
This is an open access article distributed under the Creative Commons Attribution License
MDPI and ACS Style
Kabadi, S.V.; Faden, A.I. Neuroprotective Strategies for Traumatic Brain Injury: Improving Clinical Translation. Int. J. Mol. Sci. 2014, 15, 1216-1236.
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