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Experimental traumatic brain injury

Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectively exacerbate the injury. These pathogenic injury processes are poorly understood and accordingly no effective...

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Detalles Bibliográficos
Autores principales: Albert-Weissenberger, Christiane, Sirén, Anna-Leena
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930598/
https://www.ncbi.nlm.nih.gov/pubmed/20707892
http://dx.doi.org/10.1186/2040-7378-2-16
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author Albert-Weissenberger, Christiane
Sirén, Anna-Leena
author_facet Albert-Weissenberger, Christiane
Sirén, Anna-Leena
author_sort Albert-Weissenberger, Christiane
collection PubMed
description Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectively exacerbate the injury. These pathogenic injury processes are poorly understood and accordingly no effective neuroprotective treatment is available so far. Experimental models are essential for further clarification of the highly complex pathology of traumatic brain injury towards the development of novel treatments. Among the rodent models of traumatic brain injury the most commonly used are the weight-drop, the fluid percussion, and the cortical contusion injury models. As the entire spectrum of events that might occur in traumatic brain injury cannot be covered by one single rodent model, the design and choice of a specific model represents a major challenge for neuroscientists. This review summarizes and evaluates the strengths and weaknesses of the currently available rodent models for traumatic brain injury.
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spelling pubmed-29305982010-09-01 Experimental traumatic brain injury Albert-Weissenberger, Christiane Sirén, Anna-Leena Exp Transl Stroke Med Review Traumatic brain injury, a leading cause of death and disability, is a result of an outside force causing mechanical disruption of brain tissue and delayed pathogenic events which collectively exacerbate the injury. These pathogenic injury processes are poorly understood and accordingly no effective neuroprotective treatment is available so far. Experimental models are essential for further clarification of the highly complex pathology of traumatic brain injury towards the development of novel treatments. Among the rodent models of traumatic brain injury the most commonly used are the weight-drop, the fluid percussion, and the cortical contusion injury models. As the entire spectrum of events that might occur in traumatic brain injury cannot be covered by one single rodent model, the design and choice of a specific model represents a major challenge for neuroscientists. This review summarizes and evaluates the strengths and weaknesses of the currently available rodent models for traumatic brain injury. BioMed Central 2010-08-13 /pmc/articles/PMC2930598/ /pubmed/20707892 http://dx.doi.org/10.1186/2040-7378-2-16 Text en Copyright ©2010 Albert-Weissenberger and Sirén; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Albert-Weissenberger, Christiane
Sirén, Anna-Leena
Experimental traumatic brain injury
title Experimental traumatic brain injury
title_full Experimental traumatic brain injury
title_fullStr Experimental traumatic brain injury
title_full_unstemmed Experimental traumatic brain injury
title_short Experimental traumatic brain injury
title_sort experimental traumatic brain injury
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2930598/
https://www.ncbi.nlm.nih.gov/pubmed/20707892
http://dx.doi.org/10.1186/2040-7378-2-16
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