Journal of neurotrauma
-
Journal of neurotrauma · Feb 2015
Extracellular Ezrin - a Novel Biomarker for Traumatic Brain Injury.
Traumatic brain injury (TBI) is a heterogeneous disease, and the discovery of diagnostic and prognostic TBI biomarkers is highly desirable in order to individualize patient care. We have previously published a study in which we identified possible TBI biomarkers by mass spectrometry 24 h after injury in a cell culture model. Ezrin-radixin-moesin (ERM) proteins were found abundantly in the medium after trauma, and in the present study we have identified extracellular ezrin as a possible biomarker for brain trauma by analyzing cell culture medium from injured primary neurons and glia and by measuring ezrin in cerebrospinal fluid (CSF) from both rats and humans. ⋯ Moreover, ezrin was present in all ventricular CSF samples from seven humans with severe TBI. In contrast to intracellular ezrin, which is distinctly activated following TBI, extracellular ezrin is nonphosphorylated. This is the first report of extracellular ERM proteins in human and experimental models of TBI, providing a scientific foundation for further assessment of ezrin as a potential biomarker.
-
Journal of neurotrauma · Feb 2015
Enhanced Attention Capture by Emotional Stimuli in Mild Traumatic Brain Injury.
Mild traumatic brain injury (mTBI) may be associated with compromised executive functioning and altered emotional reactivity. Despite frequent affective and cognitive symptoms in mTBI, objective evidence for brain dysfunction is often lacking. Previously we have reported compromised performance in symptomatic mTBI patients in an executive reaction time (RT) test, a computer-based RT test engaging several executive functions simultaneously. ⋯ We conclude that mTBI may be associated with enhanced attentional and executive resource allocation to threat-related stimuli. Along with behavioral evidence for enhanced attention allocation to threat stimuli, increased brain responses to threat were observed in mTBI. Enhanced attention capture by threat-related emotional stimuli may reflect inefficient top-down control of bottom-up influences of emotion, and might contribute to affective symptoms in mTBI.
-
Journal of neurotrauma · Feb 2015
Predicting institutionalization after traumatic brain injury inpatient rehabilitation.
Risk factors contributing to institutionalization after inpatient rehabilitation for people with traumatic brain injury (TBI) have not been well studied and need to be better understood to guide clinicians during rehabilitation. We aimed to develop a prognostic model that could be used at admission to inpatient rehabilitation facilities to predict discharge disposition. The model could be used to provide the interdisciplinary team with information regarding aspects of patients' functioning and/or their living situation that need particular attention during inpatient rehabilitation if institutionalization is to be avoided. ⋯ For every 10-year increment in age was associated with a 1.38 times higher risk for institutionalization (95% CI, 1.29, 1.48) and living alone was associated with a 2.34 times higher risk (95% CI, 1.86, 2.94). The c-statistic was 0.780. We conclude that this simple model can predict risk of institutionalization after inpatient rehabilitation for patients with TBI.
-
Journal of neurotrauma · Feb 2015
Mincle Signaling in the Innate Immune Response after Traumatic Brain Injury.
The innate immune response contributes to the inflammatory activity after traumatic brain injury (TBI). In the present study we identify macrophage-inducible C-type lectin (mincle) as a pattern recognition receptor that contributes to innate immunity in neurons after TBI. Here we report that mincle is activated by SAP130 in cortical neurons in culture, resulting in production of the inflammatory cytokine TNF. ⋯ Thus, these findings suggest the involvement of mincle to the pathology of TBI. Importantly, blocking mincle with a neutralizing antibody against mincle in cortical neurons in culture treated with SAP130 resulted in inhibition of mincle signaling and decreased TNF production. Therefore, our findings identify mincle as a contributor to the inflammatory response after TBI.