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Published in: Translational Stroke Research 4/2011

01-12-2011 | Review Article

Blood–Brain Barrier Pathophysiology in Traumatic Brain Injury

Authors: Adam Chodobski, Brian J. Zink, Joanna Szmydynger-Chodobska

Published in: Translational Stroke Research | Issue 4/2011

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Abstract

The blood–brain barrier (BBB) is formed by tightly connected cerebrovascular endothelial cells, but its normal function also depends on paracrine interactions between the brain endothelium and closely located glia. There is a growing consensus that brain injury, whether it is ischemic, hemorrhagic, or traumatic, leads to dysfunction of the BBB. Changes in BBB function observed after injury are thought to contribute to the loss of neural tissue and to affect the response to neuroprotective drugs. New discoveries suggest that considering the entire gliovascular unit, rather than the BBB alone, will expand our understanding of the cellular and molecular responses to traumatic brain injury (TBI). This review will address the BBB breakdown in TBI, the role of blood-borne factors in affecting the function of the gliovascular unit, changes in BBB permeability and post-traumatic edema formation, and the major pathophysiological factors associated with TBI that may contribute to post-traumatic dysfunction of the BBB. The key role of neuroinflammation and the possible effect of injury on transport mechanisms at the BBB will also be described. Finally, the potential role of the BBB as a target for therapeutic intervention through restoration of normal BBB function after injury and/or by harnessing the cerebrovascular endothelium to produce neurotrophic growth factors will be discussed.
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Metadata
Title
Blood–Brain Barrier Pathophysiology in Traumatic Brain Injury
Authors
Adam Chodobski
Brian J. Zink
Joanna Szmydynger-Chodobska
Publication date
01-12-2011
Publisher
Springer-Verlag
Published in
Translational Stroke Research / Issue 4/2011
Print ISSN: 1868-4483
Electronic ISSN: 1868-601X
DOI
https://doi.org/10.1007/s12975-011-0125-x

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