MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY
Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inf...
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doaj-33fc930bbba5492a98e6c7e77cfeefff2020-11-24T20:54:17ZengFrontiers Media S.A.Frontiers in Neurology1664-22952013-03-01410.3389/fneur.2013.0003040065MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURYDiana G Hernadez-Ontiveros0Naoki eTajiri1Sandra eAcosta2Brian eGiunta3Jun eTan4Cesar V Borlongan5University of South FloridaUniversity of South FloridaUniversity of South FloridaUniversity of South FloridaUniversity of South FloridaUniversity of South FloridaTraumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation and accurate handling of all data (Landis et al., 2012). A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI.http://journal.frontiersin.org/Journal/10.3389/fneur.2013.00030/fullMicrogliabrain imaginghead traumaanti-inflammatory therapyInflammatory Responsesecondary cell death |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Diana G Hernadez-Ontiveros Naoki eTajiri Sandra eAcosta Brian eGiunta Jun eTan Cesar V Borlongan |
spellingShingle |
Diana G Hernadez-Ontiveros Naoki eTajiri Sandra eAcosta Brian eGiunta Jun eTan Cesar V Borlongan MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY Frontiers in Neurology Microglia brain imaging head trauma anti-inflammatory therapy Inflammatory Response secondary cell death |
author_facet |
Diana G Hernadez-Ontiveros Naoki eTajiri Sandra eAcosta Brian eGiunta Jun eTan Cesar V Borlongan |
author_sort |
Diana G Hernadez-Ontiveros |
title |
MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY |
title_short |
MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY |
title_full |
MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY |
title_fullStr |
MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY |
title_full_unstemmed |
MICROGLIA ACTIVATION AS A BIOMARKER FOR TRAUMATIC BRAIN INJURY |
title_sort |
microglia activation as a biomarker for traumatic brain injury |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Neurology |
issn |
1664-2295 |
publishDate |
2013-03-01 |
description |
Traumatic brain injury (TBI) has become the signature wound of wars in Afghanistan and Iraq. Injury may result from a mechanical force, a rapid acceleration-deceleration movement, or a blast wave. A cascade of secondary cell death events ensues after the initial injury. In particular, multiple inflammatory responses accompany TBI. A series of inflammatory cytokines and chemokines spreads to normal brain areas juxtaposed to the core impacted tissue. Among the repertoire of immune cells involved, microglia is a key player in propagating inflammation to tissues neighboring the core site of injury. Neuroprotective drug trials in TBI have failed, likely due to their sole focus on abrogating neuronal cell death and ignoring the microglia response despite these inflammatory cells’ detrimental effects on the brain. Another relevant point to consider is the veracity of results of animal experiments due to deficiencies in experimental design, such as incomplete or inadequate method description, data misinterpretation and reporting may introduce bias and give false-positive results. Thus, scientific publications should follow strict guidelines that include randomization, blinding, sample-size estimation and accurate handling of all data (Landis et al., 2012). A prolonged state of inflammation after brain injury may linger for years and predispose patients to develop other neurological disorders, such as Alzheimer’s disease. TBI patients display progressive and long-lasting impairments in their physical, cognitive, behavioral, and social performance. Here, we discuss inflammatory mechanisms that accompany TBI in an effort to increase our understanding of the dynamic pathological condition as the disease evolves over time and begin to translate these findings for defining new and existing inflammation-based biomarkers and treatments for TBI. |
topic |
Microglia brain imaging head trauma anti-inflammatory therapy Inflammatory Response secondary cell death |
url |
http://journal.frontiersin.org/Journal/10.3389/fneur.2013.00030/full |
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