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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Main Authors: Diana G Hernadez-Ontiveros, Naoki eTajiri, Sandra eAcosta, Brian eGiunta, Jun eTan, Cesar V Borlongan
Format: Article
Language:English
Published: Frontiers Media S.A. 2013-03-01
Series:Frontiers in Neurology
Subjects:
Online Access:http://journal.frontiersin.org/Journal/10.3389/fneur.2013.00030/full
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spelling 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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