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Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury
Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was re...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861304/ https://www.ncbi.nlm.nih.gov/pubmed/31780883 http://dx.doi.org/10.3389/fnins.2019.01178 |
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author | Dinet, Virginie Petry, Klaus G. Badaut, Jerome |
author_facet | Dinet, Virginie Petry, Klaus G. Badaut, Jerome |
author_sort | Dinet, Virginie |
collection | PubMed |
description | Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was recognized that TBI causes significant morbidity weeks, months, or years after the initial injury, thereby contributing substantially to the overall burden of TBI and the decrease of life expectancy in these patients. Long-lasting sequels of TBI include cognitive decline/dementia, sensory-motor dysfunction, and psychiatric disorders, and most important for patients is the need for socio-economic rehabilitation affecting their quality of life. Cerebrovascular alterations have been described during the first week after TBI for direct consequence development of neuroinflammatory process in relation to brain edema. Within the brain–immune interactions, the complement system, which is a family of blood and cell surface proteins, participates in the pathophysiology process. In fact, the complement system is part of the primary defense and clearance component of innate and adaptive immune response. In this review, the complement activation after TBI will be described in relation to the activation of the microglia and astrocytes as well as the blood–brain barrier dysfunction during the first week after the injury. Considering the neuroinflammatory activity as a causal element of neurological handicaps, some major parallel lines of complement activity in multiple sclerosis and Alzheimer pathologies with regard to cognitive impairment will be discussed for chronic TBI. A better understanding of the role of complement activation could facilitate the development of new therapeutic approaches for TBI. |
format | Online Article Text |
id | pubmed-6861304 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68613042019-11-28 Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury Dinet, Virginie Petry, Klaus G. Badaut, Jerome Front Neurosci Neuroscience Traumatic brain injury (TBI) is the principal cause of death and disability in children and young adults. Clinical and preclinical research efforts have been carried out to understand the acute, life-threatening pathophysiological events happening after TBI. In the past few years, however, it was recognized that TBI causes significant morbidity weeks, months, or years after the initial injury, thereby contributing substantially to the overall burden of TBI and the decrease of life expectancy in these patients. Long-lasting sequels of TBI include cognitive decline/dementia, sensory-motor dysfunction, and psychiatric disorders, and most important for patients is the need for socio-economic rehabilitation affecting their quality of life. Cerebrovascular alterations have been described during the first week after TBI for direct consequence development of neuroinflammatory process in relation to brain edema. Within the brain–immune interactions, the complement system, which is a family of blood and cell surface proteins, participates in the pathophysiology process. In fact, the complement system is part of the primary defense and clearance component of innate and adaptive immune response. In this review, the complement activation after TBI will be described in relation to the activation of the microglia and astrocytes as well as the blood–brain barrier dysfunction during the first week after the injury. Considering the neuroinflammatory activity as a causal element of neurological handicaps, some major parallel lines of complement activity in multiple sclerosis and Alzheimer pathologies with regard to cognitive impairment will be discussed for chronic TBI. A better understanding of the role of complement activation could facilitate the development of new therapeutic approaches for TBI. Frontiers Media S.A. 2019-11-12 /pmc/articles/PMC6861304/ /pubmed/31780883 http://dx.doi.org/10.3389/fnins.2019.01178 Text en Copyright © 2019 Dinet, Petry and Badaut. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Dinet, Virginie Petry, Klaus G. Badaut, Jerome Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title_full | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title_fullStr | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title_full_unstemmed | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title_short | Brain–Immune Interactions and Neuroinflammation After Traumatic Brain Injury |
title_sort | brain–immune interactions and neuroinflammation after traumatic brain injury |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861304/ https://www.ncbi.nlm.nih.gov/pubmed/31780883 http://dx.doi.org/10.3389/fnins.2019.01178 |
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