Microglial activation in traumatic brain injury

File Description SizeFormat 
fnagi-09-00208.pdfPublished version1.72 MBAdobe PDFDownload
Title: Microglial activation in traumatic brain injury
Author(s): Donat, CK
Scott, G
Gentleman, S
Sastre, M
Item Type: Journal Article
Abstract: Microglia have a variety of functions in the brain, including synaptic pruning, CNS repair and mediating the immune response against peripheral infection. Microglia rapidly become activated in response to CNS damage. Depending on the nature of the stimulus, microglia can take a number of activation states, which correspond to altered microglia morphology, gene expression and function. It has been reported that early microglia activation following traumatic brain injury (TBI) may contribute to the restoration of homeostasis in the brain. On the other hand, if they remain chronically activated, such cells display a classically activated phenotype, releasing pro-inflammatory molecules, resulting in further tissue damage and contributing potentially to neurodegeneration. However, new evidence suggests that this classification is over-simplistic and the balance of activation states can vary at different points. In this article, we review the role of microglia in TBI, analyzing their distribution, morphology and functional phenotype over time in animal models and in humans. Animal studies have allowed genetic and pharmacological manipulations of microglia activation, in order to define their role. In addition, we describe investigations on the in vivo imaging of microglia using translocator protein (TSPO) PET and autoradiography, showing that microglial activation can occur in regions far remote from sites of focal injuries, in humans and animal models of TBI. Finally, we outline some novel potential therapeutic approaches that prime microglia/macrophages toward the beneficial restorative microglial phenotype after TBI.
Publication Date: 28-Jun-2017
Date of Acceptance: 11-Jun-2017
URI: http://hdl.handle.net/10044/1/49119
DOI: https://dx.doi.org/10.3389/fnagi.2017.00208
ISSN: 1663-4365
Publisher: Frontiers Media
Journal / Book Title: Frontiers in Aging Neuroscience
Volume: 9
Copyright Statement: © 2017 Donat, Scott, Gentleman and Sastre. 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) or licensor 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.
Sponsor/Funder: National Institutes of Health
Alzheimer's Research UK (ARUK)
Wellcome Trust
National Institutes of Health
Funder's Grant Number: 31135 (PO G130106589)
ARUK-2014NC-IMP
105603/Z/14/Z
173150
Keywords: Science & Technology
Life Sciences & Biomedicine
Geriatrics & Gerontology
Neurosciences
Neurosciences & Neurology
traumatic brain injury
CCI
microglia
neuroinflammation
TSPO
polarization states
POSITRON-EMISSION-TOMOGRAPHY
CENTRAL-NERVOUS-SYSTEM
CLOSED-HEAD INJURY
PROTEIN 18 KDA
IMPROVES FUNCTIONAL RECOVERY
18-KDA TRANSLOCATOR PROTEIN
CONTROLLED CORTICAL IMPACT
SIMPLEX-VIRUS TYPE-1
PERIPHERAL BENZODIAZEPINE
IN-VIVO
CCI
TSPO
microglia
neuroinflammation
polarization states
traumatic brain injury
Publication Status: Published
Article Number: 208
Appears in Collections:Department of Medicine
Faculty of Medicine



Items in Spiral are protected by copyright, with all rights reserved, unless otherwise indicated.

Creative Commons