Journal
PROGRESS IN NEUROBIOLOGY
Volume 95, Issue 3, Pages 352-372Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pneurobio.2011.09.003
Keywords
Traumatic brain injury; Cytokines; Inflammation; Blood brain barrier; Cerebrospinal fluid; Microdialysis
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Funding
- Medical Research Council UK [G0600986 ID79068, G9439390 ID65883]
- Royal College of Surgeons of England
- National Institute for Health Research, UK
- Raymond
- Beverley Sackler Fellowship
- University of Cambridge
- National Institute for Health Research Biomedical Research Centre, Cambridge
- Academy of Medical Sciences and the Health Foundation
- Medical Research Council [G0802251, G9439390, G0600986] Funding Source: researchfish
- National Institute for Health Research [ACF-2006-14-004] Funding Source: researchfish
- MRC [G0600986, G0802251, G9439390] Funding Source: UKRI
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There is an increasing recognition that following traumatic brain injury, a cascade of inflammatory mediators is produced, and contributes to the pathological consequences of central nervous system injury. This review summarises the key literature from pre-clinical models that underlies our understanding of innate inflammation following traumatic brain injury before focussing on the growing evidence from human studies. In addition, the underlying molecular mediators responsible for blood brain barrier dysfunction have been discussed. In particular, we have highlighted the different sampling methodologies available and the difficulties in interpreting human data of this sort. Ultimately, understanding the innate inflammatory response to traumatic brain injury may provide a therapeutic avenue in the treatment of central nervous system disease. (C) 2011 Elsevier Ltd. All rights reserved.
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