scholarly journals Sex-Differences in Traumatic Brain Injury in the Absence of Tau in Drosophila

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 917
Author(s):  
Ekta J. Shah ◽  
Katherine Gurdziel ◽  
Douglas M. Ruden
Keyword(s):  
Traumatic Brain Injury ◽  
Sex Differences ◽  
Brain Injury ◽  
Brain Injuries ◽  
Chronic Traumatic Encephalopathy ◽  
Brain Area ◽  
Subsequent Development ◽  
Gene Transcript ◽  
Post Injury ◽  
Knock Out

Traumatic brain injuries, a leading cause of death and disability worldwide, are caused by a severe impact to the head that impairs physiological and psychological function. In addition to severity, type and brain area affected, brain injury outcome is also influenced by the biological sex of the patient. Traumatic brain injury triggers accumulation of Tau protein and the subsequent development of Tauopathies, including Alzheimer’s disease and Chronic traumatic encephalopathy. Recent studies report differences in Tau network connections between healthy males and females, but the possible role of Tau in sex-dependent outcome to brain injury is unclear. Thus, we aimed to determine if Tau ablation would alleviate sex dependent outcomes in injured flies. We first assessed motor function and survival in tau knock-out flies and observed sex-differences in climbing ability, but no change in locomotor activity in either sex post-injury. Sex differences in survival time were also observed in injured tau deficient flies with a dramatically higher percent of female death within 24 h than males. Additionally, 3′mRNA-Seq studies in isolated fly brains found that tau deficient males show more gene transcript changes than females post-injury. Our results suggest that sex differences in TBI outcome and recovery are not dependent on the presence of Tau in Drosophila.

scholarly journals Traumatic glioblastoma: commentary and suggested mechanism

2018 ◽  
Vol 46 (6) ◽  
pp. 2170-2176
Author(s):  
Nissim Ohana ◽  
Daniel Benharroch ◽  
Dimitri Sheinis ◽  
Abraham Cohen
Keyword(s):  
Traumatic Brain Injury ◽  
Transcription Factors ◽  
Brain Injury ◽  
Brain Injuries ◽  
Hypoxia Inducible Factor ◽  
Subsequent Development ◽  
Factors Associated ◽  
The Relationship

The role of head trauma in the development of glioblastoma is highly controversial and has been minimized since first put forward. This is not unexpected because skull injuries are overwhelmingly more common than glioblastoma. This paper presents a commentary based on the contributions of James Ewing, who established a major set of criteria for the recognition of an official relationship between trauma and cancer. Ewing’s criteria were very stringent. The scholars who succeeded Ewing have facilitated the characterization of traumatic brain injuries since the introduction of computed tomography and magnetic resonance imaging. Discussions of the various criteria that have since developed are now being conducted, and those of an unnecessarily limiting nature are being highlighted. Three transcription factors associated with traumatic brain injury have been identified: p53, hypoxia-inducible factor-1α, and c-MYC. A role for these three transcription factors in the relationship between traumatic brain injury and glioblastoma is suggested; this role may support a cause-and-effect link with the subsequent development of glioblastoma.

281 Predicting neurodegeneration after traumatic brain injury

2018 ◽  
Vol 89 (10) ◽  
pp. A42.1-A42
Author(s):  
Graham Neil SN ◽  
Jolly Amy E ◽  
Bourke Niall J ◽  
Scott Gregory ◽  
Cole James H ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
White Matter ◽  
Brain Atrophy ◽  
Diffusion Tensor ◽  
Chronic Traumatic Encephalopathy ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Jacobian Determinant ◽  
Post Injury

BackgroundDementia rates are elevated after traumatic brain injury (TBI) and a subgroup develops chronic traumatic encephalopathy. Post-traumatic neurodegeneration can be measured by brain atrophy rates derived from neuroimaging, but it is unclear how atrophy relates to the initial pattern of injury.ObjectivesTo investigate the relationship between baseline TBI patterns and subsequent neurodegeneration measured by progressive brain atrophy.Methods55 patients after moderate-severe TBI (mean 3 years post-injury) and 20 controls underwent longitudinal MRI. Brain atrophy was quantified using the Jacobian determinant defined from volumetric T1 scans approximately one year apart. Diffuse axonal injury was measured using diffusion tensor imaging and focal injuries defined from T1 and FLAIR. Neuropsychological assessment was performed.ResultsAbnormal progressive brain atrophy was seen after TBI (~1.8%/year in white matter). This was accompanied by widespread reductions in fractional anisotropy, in keeping with the presence of diffuse axonal injury. There was a strong negative correlation between FA and brain atrophy, whereby areas of greater white matter damage showed greater atrophy over time.ConclusionsThe results show a strong relationship between the location of diffuse axonal injury and subsequent neurodegeneration. This suggests that TBI triggers progressive neurodegeneration through the long-lasting effects of diffuse axonal injury.

Predictors of 1-Month and 1-Year Neurocognitive Functioning from the UCLA Longitudinal Mild, Uncomplicated, Pediatric Traumatic Brain Injury Study

2012 ◽  
Vol 19 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Talin Babikian ◽  
David McArthur ◽  
Robert F. Asarnow
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Parental Education ◽  
Brain Injuries ◽  
Injury Severity ◽  
School Achievement ◽  
Body Part ◽  
Neurocognitive Deficits ◽  
Post Injury ◽  
Neurocognitive Impairments

AbstractAlthough more severe brain injuries have long been associated with persisting neurocognitive deficits, an increasing body of literature has shown that children/adolescents with single, uncomplicated mild traumatic brain injury (mTBI) do not exhibit long-lasting neurocognitive impairments. Nonetheless, clinical experience and our previous report (Babikian, 2011) showed that a minority of children/adolescents exhibit persistent cognitive problems using performance based measures following what appear to be relatively mild injuries. Predictors of poor neurocognitive outcomes were evaluated in 76 mTBI and 79 Other Injury subjects to determine the relative contributions of indices of injury severity, clinical symptomatology, demographic factors, and premorbid functioning in predicting 1-month and 12-month neurocognitive impairment on computerized or paper and pencil measures. Injury severity indicators or type of injury (head vs. other body part) did not predict either 1-month or 12-month cognitive impairment status. Rather, premorbid variables that antedated the injury (parental education, premorbid behavior and/or learning problems, and school achievement) predicted cognitive impairments. When post-injury neurocognitive impairments are observed in survivors of mild injuries (head or other body part), a sound understanding of their etiology is critical in designing appropriate intervention plans. Clinical and research implications are discussed. (JINS, 2012, 18, 1–10)

scholarly journals Analysis of Neuron Specific Enolase Serum Levels in Traumatic Brain Injury

2021 ◽  
Vol 5 (4) ◽  
pp. 1218-1222
Author(s):  
Yuliarni Syafrita ◽  
Nora Fitri
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Injuries ◽  
Neuron Specific Enolase ◽  
Serum Levels ◽  
Pathological Process ◽  
P Value ◽  
Secondary Brain Injury ◽  
Post Injury ◽  
The Brain

Background : Traumatic brain injury is still the main cause of death and disability in productive age. Assessment the level of consciousness and imaging examinations after a brain injury can not always describe the severity of damage in the brain, this is because the pathological process is still ongoing due to secondary brain injury. Therefore, it is necessary to examine biomarkers that can describe the severity of the pathological process that occurs. The purpose of this study was to assess serum neuron-specific enolase (NSE) levels and their relationship to the severity and outcome of a traumatic brain injury. Methods : A cross sectional design was conducted in the emergency department of DR M Djamil Hospital, Padang. There were 72 patients who met the inclusion criteria. A Glasgow Coma Scale examination was performed to assess the severity of brain injury and examination of NSE serum levels at 48 hours post- injury using ELISA technique and assess the Glasgow outcome scale (GOS) at 6 weeks post-injury. Data analysis using SPSS 22 program, the results are significance if the p value <0.05  Results : The average NSE level was higher in severe brain injuries than moderate and mild brain injuries and this difference was statistically significant (p<0.05).  The NSE serum levels were higher in poor outcomes than in good outcomes and this difference was statistically significant (p<0.05).  Conclusion : High NSE serum levels in the acute phase were associated with the severity of the brain injury and poor outcome 6 weeks after the brain injury. 

scholarly journals Low-Level Primary Blast Induces Neuroinflammation and Neurodegeneration in Rats

2019 ◽  
Vol 184 (Supplement_1) ◽  
pp. 265-272 ◽  
Author(s):  
Yansong Li ◽  
Zhangsheng Yang ◽  
Bin Liu ◽  
Celina Valdez ◽  
Mikulas Chavko ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neuronal Degeneration ◽  
Chronic Traumatic Encephalopathy ◽  
Inflammatory Cells ◽  
Post Traumatic Stress ◽  
Post Injury ◽  
Blast Overpressure ◽  
Blast Traumatic Brain Injury ◽  
Combat Casualty

AbstractObjectiveMild blast traumatic brain injury is commonly prevalent in modern combat casualty care and has been associated with the development of neurodegenerative conditions. However, whether primary lower level blast overpressure (LBOP) causes neurodegeneration and neuroinflammation remains largely unknown. The aim of our present study was to determine whether LBOP can cause neuroinflammation and neurodegeneration.MethodsAnesthetized rats were randomly assigned to LBOP group (70 kPa, n = 5) or sham group (without blast, n = 5). Histopathological and cytokine changes in brain tissue at 5 days post-injury were evaluated by hematoxylin-eosin staining and Bioplex assay, respectively.ResultsHistopathological assessment revealed neuronal degeneration and increased density of inflammatory cells in frontal and parietal cortex, hippocampus and thalamus in rats exposed to LBOP. LBOP exposure significantly elevated levels of pro-inflammatory cytokines (EPO, IL-1β, IL-6, IL-12, IL-18, and TNF-α) and chemokines (GRO and RANTES) as well as of an anti-inflammatory cytokine (IL-13) in the frontal cortex.ConclusionsThis study reveals a role of neuroinflammation in neurodegeneration after mild blast traumatic brain injury. Therapies that target this process might in warfighters might function either by attenuating the development of post-traumatic stress disorder, chronic traumatic encephalopathy and Alzheimer’s disease, or by slowing their progression.

scholarly journals Investigating the cumulative effects of Δ9-tetrahydrocannabinol and repetitive mild traumatic brain injury on adolescent rats

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Dhyey Bhatt ◽  
Ali Hazari ◽  
Glenn R Yamakawa ◽  
Sabrina Salberg ◽  
Marissa Sgro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Prefrontal Cortex ◽  
Brain Injury ◽  
Nucleus Accumbens ◽  
Mild Traumatic Brain Injury ◽  
Brain Injuries ◽  
Therapeutic Benefit ◽  
Sprague Dawley ◽  
Post Injury ◽  
Beneficial Effects

Abstract The prevalence of mild traumatic brain injury is highest amongst the adolescent population and can lead to complications including neuroinflammation and excitotoxicity. Also pervasive in adolescents is recreational cannabis use. Δ9-Tetrahydrocannabinol, the main psychoactive component of cannabis, is known to have anti-inflammatory properties and serves as a neuroprotective agent against excitotoxicity. Thus, we investigated the effects of Δ9-tetrahydrocannabinol on recovery when administered either prior to or following repeated mild brain injuries. Male and female Sprague-Dawley rats were randomly assigned to receive Δ9-tetrahydrocannabinol or vehicle either prior to or following the repeated injuries. Rats were then tested on a behavioural test battery designed to measure post-concussive symptomology. The hippocampus, nucleus accumbens and prefrontal cortex were extracted from all animals to examine mRNA expression changes (Bdnf, Cnr1, Comt, GR, Iba-1 and Vegf-2R). We hypothesized that, in both experiments, Δ9-tetrahydrocannabinol administration would provide neuroprotection against mild injury outcomes and confer therapeutic benefit. Δ9-Tetrahydrocannabinol administration following repeated mild traumatic brain injury was beneficial to three of the six behavioural outcomes affected by injury (reducing anxiety and depressive-like behaviours while also mitigating injury-induced deficits in short-term working memory). Δ9-Tetrahydrocannabinol administration following injury also showed beneficial effects on the expression of Cnr1, Comt and Vegf-2R in the hippocampus, nucleus accumbens and prefrontal cortex. There were no notable benefits of Δ9-tetrahydrocannabinol when administered prior to injury, suggesting that Δ9-tetrahydrocannabinol may have potential therapeutic benefit on post-concussive symptomology when administered post-injury, but not pre-injury.

scholarly journals Longitudinal assessment of hemodynamic alterations after mild traumatic brain injury in adolescents: Selected case study review

2022 ◽  
Vol 6 ◽  
pp. 205970022110658
Author(s):  
Corey M. Thibeault ◽  
Amber Y. Dorn ◽  
Shankar Radhakrishnan ◽  
Robert B. Hamilton
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Injuries ◽  
Population Level ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Breath Hold ◽  
Longitudinal Assessment ◽  
Post Injury ◽  
Cross Sectional

Alterations in the neurovasculature after traumatic brain injury (TBI) represents a significant sequelae. However, despite theoretical and empirical evidence supporting the near-ubiquity of vascular injury, its pathophysiology remains elusive. Although this has been shown for all grades of TBI, the vascular changes after injuries with the broad mild traumatic brain injuries (mTBI) classification, remain particularly difficult to describe. Our group has previously demonstrated hemodynamic alterations in mTBI by utilizing transcranial Doppler ultrasound and cerebrovascular reactivity in a cross-sectional study. That work identified a phasic progression of deviations over varying days post-injury. These phases were then characterized by a set of inverse models that provided a hypothetical process of hemodynamic dysfunction after mTBI. This model set provides a framework with the potential for guiding clinical treatment over the course of recovery. However, it is still unclear if individual patients will progress through the phases of dysfunction similar to that found at the population level. The work presented here explores six individual patients with high-density data collected during their post-injury recovery. Breath-hold index (BHI) was found to be the most robust feature related to mTBI longitudinally. All six subjects exhibited BHI recovery curves that followed the population model's progression. The changes in pulsatile features lacked the universality of BHI, but were present in subjects with higher self-reported symptom scores and longer periods of recovery. This work suggests neurovascular dysfunction after an mTBI may be a robust phenomenon. Additionally, the capabilities of TCD in capturing these changes highlights its potential for aiding clinicians in monitoring patient's recovery post mTBI.

MANAGEMENT OF MULTIPLE TRAUMATIC INTRACRANIAL HEMATOMAS

2020 ◽  
Vol 3 (1) ◽  
pp. 70-74
Author(s):  
Rustam Hazratkulov ◽  
Keyword(s):  
Traumatic Brain Injury ◽  
Surgical Treatment ◽  
Brain Injury ◽  
Hospital Stay ◽  
Treatment Outcomes ◽  
Brain Injuries ◽  
Traumatic Brain Injuries ◽  
Diagnostic Approach ◽  
Early Activation ◽  
Intracranial Hematomas

Multiple traumatic hematomas (MG) account for 0.74% of all traumatic brain injuries. A comprehensive diagnostic approach to multiple traumatic intracranial hematomas allows to establish a diagnosis in the early stages of traumatic brain injury and to determine treatment tactics. A differentiated approach to the choice of surgical treatment of multiple hematomas allows to achieve satisfactory results and treatment outcomes, which accordingly contributes to the early activation of the patient, a reduction in hospital stay, a decrease in mortality and disabilityin patients with traumatic brain injury

scholarly journals A-126 Clinical Utility of Risk Factors to Predict Self-reported Neurobehavioral Outcome Following Traumatic Brain Injury: PTSD, Sleep, Resilience, and Lifetime Blast Exposure

2020 ◽  
Vol 35 (6) ◽  
pp. 919-919
Author(s):  
Lange R ◽  
Lippa S ◽  
Hungerford L ◽  
Bailie J ◽  
French L ◽  
...  
Keyword(s):  
Risk Factors ◽  
Traumatic Brain Injury ◽  
Risk Factor ◽  
Brain Injury ◽  
Clinical Utility ◽  
Poor Sleep ◽  
Post Injury ◽  
Poor Outcome ◽  
Blast Exposure ◽  
Neurobehavioral Outcome

Abstract Objective To examine the clinical utility of PTSD, Sleep, Resilience, and Lifetime Blast Exposure as ‘Risk Factors’ for predicting poor neurobehavioral outcome following traumatic brain injury (TBI). Methods Participants were 993 service members/veterans evaluated following an uncomplicated mild TBI (MTBI), moderate–severe TBI (ModSevTBI), or injury without TBI (Injured Controls; IC); divided into three cohorts: (1) &lt; 12 months post-injury, n = 237 [107 MTBI, 71 ModSevTBI, 59 IC]; (2) 3-years post-injury, n = 370 [162 MTBI, 80 ModSevTBI, 128 IC]; and (3) 10-years post-injury, n = 386 [182 MTBI, 85 ModSevTBI, 119 IC]. Participants completed a 2-hour neurobehavioral test battery. Odds Ratios (OR) were calculated to determine whether the ‘Risk Factors’ could predict ‘Poor Outcome’ in each cohort separately. Sixteen Risk Factors were examined using all possible combinations of the four risk factor variables. Poor Outcome was defined as three or more low scores (&lt; 1SD) on five TBI-QOL scales (e.g., Fatigue, Depression). Results In all cohorts, the vast majority of risk factor combinations resulted in ORs that were ‘clinically meaningful’ (ORs &gt; 3.00; range = 3.15 to 32.63, all p’s &lt; .001). Risk factor combinations with the highest ORs in each cohort were PTSD (Cohort 1 & 2, ORs = 17.76 and 25.31), PTSD+Sleep (Cohort 1 & 2, ORs = 18.44 and 21.18), PTSD+Sleep+Resilience (Cohort 1, 2, & 3, ORs = 13.56, 14.04, and 20.08), Resilience (Cohort 3, OR = 32.63), and PTSD+Resilience (Cohort 3, OR = 24.74). Conclusions Singularly, or in combination, PTSD, Poor Sleep, and Low Resilience were strong predictors of poor outcome following TBI of all severities and injury without TBI. These variables may be valuable risk factors for targeted early interventions following injury.

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