scholarly journals Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast-Induced Traumatic Brain Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Xiaoping Du ◽  
Matthew B. West ◽  
Weihua Cheng ◽  
Donald L. Ewert ◽  
Wei Li ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Auditory Pathway ◽  
Antioxidant Treatment ◽  
Tertiary Butyl ◽  
Early Onset Dementia ◽  
Mossy Cells ◽  
Blast Overpressure ◽  
Promising Therapeutic Approach ◽  
Central Auditory Pathway

Traumatic brain injury (TBI) can lead to early onset dementia and other related neurodegenerative diseases. We previously demonstrated that damage to the central auditory pathway resulting from blast-induced TBI (bTBI) could be significantly attenuated by a combinatorial antioxidant treatment regimen. In the current study, we examined the localization patterns of normal Tau and the potential blast-induced accumulation of neurotoxic variants of this microtubule-associated protein that are believed to potentiate the neurodegenerative effects associated with synaptic dysfunction in the hippocampus following three successive blast overpressure exposures in nontransgenic rats. We observed a marked increase in the number of both hyperphosphorylated and oligomeric Tau-positive hilar mossy cells and somatic accumulation of endogenous Tau in oligodendrocytes in the hippocampus. Remarkably, a combinatorial regimen of 2,4-disulfonylα-phenyl tertiary butyl nitrone (HPN-07) andN-acetylcysteine (NAC) resulted in striking reductions in the numbers of both mossy cells and oligodendrocytes positively labeled for these pathological Tau immunoreactivity patterns in response to bTBI. This treatment strategy represents a promising therapeutic approach for simultaneously reducing or eliminating both primary auditory injury and nonauditory changes associated with bTBI-induced hippocampal neurodegeneration.

scholarly journals Mild traumatic brain injury induced by primary blast overpressure produces dynamic regional changes in [18F]FDG uptake

2019 ◽  
Vol 1723 ◽  
pp. 146400 ◽  
Author(s):  
Shalini Jaiswal ◽  
Andrew K. Knutsen ◽  
Colin M. Wilson ◽  
Amanda H. Fu ◽  
Laura B. Tucker ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Primary Blast ◽  
Fdg Uptake ◽  
Blast Overpressure ◽  
18F Fdg

scholarly journals Blast-Related Traumatic Brain Injury: Current Concepts and Research Considerations

2019 ◽  
Vol 13 ◽  
pp. 117906951987221 ◽  
Author(s):  
Daniel W Bryden ◽  
Jessica I Tilghman ◽  
Sidney R Hinds
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Trauma ◽  
Department Of Defense ◽  
Military Service ◽  
The Body ◽  
Us Army ◽  
Blast Overpressure ◽  
Wide Variability ◽  
Injury Severities

Traumatic brain injury (TBI) is a well-known consequence of participation in activities such as military combat or collision sports. But the wide variability in eliciting circumstances and injury severities makes the study of TBI as a uniform disease state impossible. Military Service members are under additional, unique threats such as exposure to explosive blast and its unique effects on the body. This review is aimed toward TBI researchers, as it covers important concepts and considerations for studying blast-induced head trauma. These include the comparability of blast-induced head trauma to other mechanisms of TBI, whether blast overpressure induces measureable biomarkers, and whether a biodosimeter can link blast exposure to health outcomes, using acute radiation exposure as a corollary. This examination is contextualized by the understanding of concussive events and their psychological effects throughout the past century’s wars, as well as the variables that predict sustaining a TBI and those that precipitate or exacerbate psychological conditions. Disclaimer: The views expressed in this article are solely the views of the authors and not those of the Department of Defense Blast Injury Research Coordinating Office, US Army Medical Research and Development Command, US Army Futures Command, US Army, or the Department of Defense.

scholarly journals Traumatic Brain Injury and Delayed Sequelae: A Review - Traumatic Brain Injury and Mild Traumatic Brain Injury (Concussion) are Precursors to Later-Onset Brain Disorders, Including Early-Onset Dementia

2007 ◽  
Vol 7 ◽  
pp. 1768-1776 ◽  
Author(s):  
Michael A. Kiraly ◽  
Stephen J. Kiraly
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Brain Injuries ◽  
Brain Disorders ◽  
Early Onset Dementia ◽  
Human Experiments ◽  
Delayed Consequences ◽  
Subsequent Onset

Brain injuries are too common. Most people are unaware of the incidence of and horrendous consequences of traumatic brain injury (TBI) and mild traumatic brain injury (MTBI). Research and the advent of sophisticated imaging have led to progression in the understanding of brain pathophysiology following TBI. Seminal evidence from animal and human experiments demonstrate links between TBI and the subsequent onset of premature, psychiatric syndromes and neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Objectives of this summary are, therefore, to instill appreciation regarding the importance of brain injury prevention, diagnosis, and treatment, and to increase awareness regarding the long-term delayed consequences following TBI.

scholarly journals Traumatic brain injury induced by exposure to blast overpressure via ear canal

2022 ◽  
Vol 17 (1) ◽  
pp. 115
Author(s):  
Yi Pang ◽  
Hong Zhu ◽  
Yang Ou ◽  
BradA Clifton ◽  
Jinghui Li ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Ear Canal ◽  
Blast Overpressure

scholarly journals Exosome Derived From Traumatic Brain Injury Patients Accelerates Fracture Healing via SMAD7 Signaling Regulation

2021 ◽  
Author(s):  
Yuan Xiong ◽  
Ze Lin ◽  
Hang Xue ◽  
Yiqiang Hu ◽  
Tao Yu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Beneficial Effect ◽  
Fracture Healing ◽  
Osteogenic Differentiation ◽  
Alizarin Red ◽  
Knock Down ◽  
Beneficial Role ◽  
Promising Therapeutic Approach

Abstract BackgroundExtremity injuries, especially for bone fracture, predominate in warfare, and around one-third of military personnel sustain at least one kind of traumatic brain injury (TBI). The beneficial role of TBI in osteogenic differentiation and fracture healing was found in clinic, however, the underlying mechanism of this interesting finding is elusive. Exosome (Exos) is nanosized extracellular vesicles, and their regulatory role in bone remodeling have attracted accumulative attention.MethodsUltra-high speed gradient centrifugation was used to extract exosomes (Exos) both from fracture patients combined with TBI (TBI-Exos), and from isolated fracture patients (Ctr-Exos). Human mesenchymal stem cells (hMSCs) proliferation was checked by qRT-PCR, western blotting, ALP staining, alizarin red staining, and EdU (5-ethynyl-2’-deoxyuridine) assays. In addition, C57BL/6J mice were randomly divided into different groups according to the treatments, and the radiographic and histopathological results were analyzed to evaluate the effect of TBI-Exos on fracture healing. ResultsIn vitro, suppression of SMAD7 promoted osteogenic differentiation, whereas knock down of miR-21-5p in TBI-Exos deprived this bone-beneficial effect at a great extent. Similarly, our results confirmed that pre-injection of TBI-Exos leads to enhanced bone formation, whereas knock down of exosomal miR-21-5p was capable to markedly impair this bone-beneficial effect in vivo. ConclusionOur findings provide a potential mechanism of the beneficial role of TBI in fracture healing with a particular focus on the TBI-Exos, and suggest that the use of nanosized materials combined with miR-21-5p-mimics may be a promising therapeutic approach to enhance fracture healing in the future.

Significant Head Accelerations Can Influence Immediate Neurological Impairments in a Murine Model of Blast-Induced Traumatic Brain Injury

2014 ◽  
Vol 136 (9) ◽  
Author(s):  
David M. Gullotti ◽  
Matthew Beamer ◽  
Matthew B. Panzer ◽  
Yung Chia Chen ◽  
Tapan P. Patel ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Shock Tube ◽  
High Speed ◽  
Biochemical Characterization ◽  
Chronic Traumatic Encephalopathy ◽  
Military Population ◽  
Pressure Transducers ◽  
Blast Overpressure ◽  
Blast Neurotrauma

Although blast-induced traumatic brain injury (bTBI) is well recognized for its significance in the military population, the unique mechanisms of primary bTBI remain undefined. Animate models of primary bTBI are critical for determining these potentially unique mechanisms, but the biomechanical characteristics of many bTBI models are poorly understood. In this study, we examine some common shock tube configurations used to study blast-induced brain injury in the laboratory and define the optimal configuration to minimize the effect of torso overpressure and blast-induced head accelerations. Pressure transducers indicated that a customized animal holder successfully reduced peak torso overpressures to safe levels across all tested configurations. However, high speed video imaging acquired during the blast showed significant head accelerations occurred when animals were oriented perpendicular to the shock tube axis. These findings of complex head motions during blast are similar to previous reports [Goldstein et al., 2012, “Chronic Traumatic Encephalopathy in Blast-Exposed Military Veterans and a Blast Neurotrauma Mouse Model,” Sci. Transl. Med., 4(134), 134ra160; Sundaramurthy et al., 2012, “Blast-Induced Biomechanical Loading of the Rat: An Experimental and Anatomically Accurate Computational Blast Injury Model,” J. Neurotrauma, 29(13), pp. 2352–2364; Svetlov et al., 2010, “Morphologic and Biochemical Characterization of Brain Injury in a Model of Controlled Blast Overpressure Exposure,” J. Trauma, 69(4), pp. 795–804]. Under the same blast input conditions, minimizing head acceleration led to a corresponding elimination of righting time deficits. However, we could still achieve righting time deficits under minimal acceleration conditions by significantly increasing the peak blast overpressure. Together, these data show the importance of characterizing the effect of blast overpressure on head kinematics, with the goal of producing models focused on understanding the effects of blast overpressure on the brain without the complicating factor of superimposed head accelerations.

scholarly journals Blast overpressure induces shear-related injuries in the brain of rats exposed to a mild traumatic brain injury

2013 ◽  
Vol 1 (1) ◽  
Author(s):  
Miguel A Gama Sosa ◽  
Rita De Gasperi ◽  
Alejandro J Paulino ◽  
Paul E Pricop ◽  
Michael C Shaughness ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Blast Overpressure ◽  
The Brain

scholarly journals Astrocytes Mediate Protective Actions of Estrogenic Compounds after Traumatic Brain Injury

2018 ◽  
Vol 108 (2) ◽  
pp. 142-160 ◽  
Author(s):  
Cynthia Martin-Jiménez ◽  
Diana Milena Gaitán-Vaca ◽  
Natalia Areiza ◽  
Valentina Echeverria ◽  
Ghulam Md Ashraf ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Therapeutic Approach ◽  
Public Health Problem ◽  
Current Evidence ◽  
Protective Mechanisms ◽  
Estrogenic Compounds ◽  
Protective Actions ◽  
Promising Therapeutic Approach ◽  
Synthetic Estrogens

Traumatic brain injury (TBI) is a serious public health problem. It may result in severe neurological disabilities and in a variety of cellular metabolic alterations for which available therapeutic strategies are limited. In the last decade, the use of estrogenic compounds, which activate protective mechanisms in astrocytes, has been explored as a potential experimental therapeutic approach. Previous works have suggested estradiol (E2) as a neuroprotective hormone that acts in the brain by binding to estrogen receptors (ERs). Several steroidal and nonsteroidal estrogenic compounds can imitate the effects of estradiol on ERs. These include hormonal estrogens, phytoestrogens and synthetic estrogens, such as selective ER modulators or tibolone. Current evidence of the role of astrocytes in mediating protective actions of estrogenic compounds after TBI is reviewed in this paper. We conclude that the use of estrogenic compounds to modulate astrocytic properties is a promising therapeutic approach for the treatment of TBI.

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.

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