Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, n...

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Autores principales:	Ralph Timaru-Kast, Clara Luh, Philipp Gotthardt, Changsheng Huang, Michael K Schäfer, Kristin Engelhard, Serge C Thal
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/c527921eb9924d529e9034bacb3e0a8a
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spelling	oai:doaj.org-article:c527921eb9924d529e9034bacb3e0a8a2021-11-18T07:07:03ZInfluence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.1932-620310.1371/journal.pone.0043829https://doaj.org/article/c527921eb9924d529e9034bacb3e0a8a2012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22952778/?tool=EBIhttps://doaj.org/toc/1932-6203After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count) were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2%) compared to young (0%). This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral inflammation without major differences in morphological brain damage compared to young.Ralph Timaru-KastClara LuhPhilipp GotthardtChangsheng HuangMichael K SchäferKristin EngelhardSerge C ThalPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 8, p e43829 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ralph Timaru-Kast Clara Luh Philipp Gotthardt Changsheng Huang Michael K Schäfer Kristin Engelhard Serge C Thal Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
description	After traumatic brain injury (TBI) elderly patients suffer from higher mortality rate and worse functional outcome compared to young patients. However, experimental TBI research is primarily performed in young animals. Aim of the present study was to clarify whether age affects functional outcome, neuroinflammation and secondary brain damage after brain trauma in mice. Young (2 months) and old (21 months) male C57Bl6N mice were anesthetized and subjected to a controlled cortical impact injury (CCI) on the right parietal cortex. Animals of both ages were randomly assigned to 15 min, 24 h, and 72 h survival. At the end of the observation periods, contusion volume, brain water content, neurologic function, cerebral and systemic inflammation (CD3+ T cell migration, inflammatory cytokine expression in brain and lung, blood differential cell count) were determined. Old animals showed worse neurological function 72 h after CCI and a high mortality rate (19.2%) compared to young (0%). This did not correlate with histopathological damage, as contusion volumes were equal in both age groups. Although a more pronounced brain edema formation was detected in old mice 24 hours after TBI, lack of correlation between brain water content and neurological deficit indicated that brain edema formation is not solely responsible for age-dependent differences in neurological outcome. Brains of old naïve mice were about 8% smaller compared to young naïve brains, suggesting age-related brain atrophy with possible decline in plasticity. Onset of cerebral inflammation started earlier and primarily ipsilateral to damage in old mice, whereas in young mice inflammation was delayed and present in both hemispheres with a characteristic T cell migration pattern. Pulmonary interleukin 1β expression was up-regulated after cerebral injury only in young, not aged mice. The results therefore indicate that old animals are prone to functional deficits and strong ipsilateral cerebral inflammation without major differences in morphological brain damage compared to young.
format	article
author	Ralph Timaru-Kast Clara Luh Philipp Gotthardt Changsheng Huang Michael K Schäfer Kristin Engelhard Serge C Thal
author_facet	Ralph Timaru-Kast Clara Luh Philipp Gotthardt Changsheng Huang Michael K Schäfer Kristin Engelhard Serge C Thal
author_sort	Ralph Timaru-Kast
title	Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
title_short	Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
title_full	Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
title_fullStr	Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
title_full_unstemmed	Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
title_sort	influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/c527921eb9924d529e9034bacb3e0a8a
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Influence of age on brain edema formation, secondary brain damage and inflammatory response after brain trauma in mice.

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