The contribution of astrocytes and microglia to traumatic brain injury

Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. Brain injuries are highly heterogeneous and can also trigger other neurological complications, including epilepsy, depression and dementia. The initial injury often leads to the development of secon...

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Vydané v:British journal of pharmacology Ročník 173; číslo 4; s. 692 - 702
Hlavní autori: Karve, Ila P, Taylor, Juliet M, Crack, Peter J
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Blackwell Publishing Ltd 01.02.2016
John Wiley and Sons Inc
Predmet:
Animal models
Animals
Astrocytes
Astrocytes - pathology
Brain Injuries, Traumatic - pathology
Brain Injuries, Traumatic - physiopathology
Cell death
Central nervous system
Chemokines
Cytokines
Cytotoxicity
Dementia disorders
Edema
Epilepsy
Growth factors
Humans
Hypoxia
Inflammation
Inflammation - pathology
Inflammation - physiopathology
Ischemia
Mental depression
Microglia
Microglia - pathology
Molecular modelling
Neurodegeneration
Neurological complications
Oxidative stress
Review
Themed Section: Reviews
Traumatic brain injury
ISSN:0007-1188, 1476-5381, 1476-5381
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Popis
Shrnutí:Traumatic brain injury (TBI) represents a major cause of death and disability in developed countries. Brain injuries are highly heterogeneous and can also trigger other neurological complications, including epilepsy, depression and dementia. The initial injury often leads to the development of secondary sequelae; cellular hyperexcitability, vasogenic and cytotoxic oedema, hypoxia‐ischaemia, oxidative stress and inflammation, all of which influence expansion of the primary lesion. It is widely known that inflammatory events in the brain following TBI contribute to the widespread cell death and chronic tissue degeneration. Neuroinflammation is a multifaceted response involving a number of cell types, both within the CNS and in the peripheral circulation. Astrocytes and microglia, cells of the CNS, are considered key players in initiating an inflammatory response after injury. These cells are capable of secreting various cytokines, chemokines and growth factors, and following injury to the CNS, undergo changes in morphology. Ultimately, these changes can influence the local microenvironment and thus determine the extent of damage and subsequent repair. This review will focus on the roles of microglia and astrocytes following TBI, highlighting some of the key processes, pathways and mediators involved in this response. Additionally, both the beneficial and the detrimental aspects of these cellular responses will be examined using evidence from animal models and human post‐mortem TBI studies. Linked Articles This article is part of a themed section on Inflammation: maladies, models, mechanisms and molecules. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2016.173.issue-4
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ISSN:0007-1188
1476-5381
1476-5381
DOI:10.1111/bph.13125