scholarly journals Hericium erinaceus and Coriolus versicolor Modulate Molecular and Biochemical Changes after Traumatic Brain Injury

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 898
Author(s):  
Ramona D’Amico ◽  
Angela Trovato Salinaro ◽  
Roberta Fusco ◽  
Marika Cordaro ◽  
Daniela Impellizzeri ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Oral Treatment ◽  
Coriolus Versicolor ◽  
Strong Increase ◽  
Functional Impairments ◽  
Physical Force ◽  
Hericium Erinaceus ◽  
The Impact ◽  
The Brain

Traumatic brain injury (TBI) is a major health and socioeconomic problem affecting the world. This condition results from the application of external physical force to the brain which leads to transient or permanent structural and functional impairments. TBI has been shown to be a risk factor for neurodegeneration which can lead to Parkinson’s disease (PD) for example. In this study, we wanted to explore the development of PD-related pathology in the context of an experimental model of TBI and the potential ability of Coriolus versicolor and Hericium erinaceus to prevent neurodegenerative processes. Traumatic brain injury was induced in mice by controlled cortical impact. Behavioral tests were performed at various times: the animals were sacrificed 30 days after the impact and the brain was processed for Western blot and immunohistochemical analyzes. After the head injury, a significant decrease in the expression of tyrosine hydroxylase and the dopamine transporter in the substantia nigra was observed, as well as significant behavioral alterations that were instead restored following daily oral treatment with Hericium erinaceus and Coriolus versicolor. Furthermore, a strong increase in neuroinflammation and oxidative stress emerged in the vehicle groups. Treatment with Hericium erinaceus and Coriolus versicolor was able to prevent both the neuroinflammatory and oxidative processes typical of PD. This study suggests that PD-related molecular events may be triggered on TBI and that nutritional fungi such as Hericium erinaceus and Coriolus versicolor may be important in redox stress response mechanisms and neuroprotection, preventing the progression of neurodegenerative diseases such as PD.

Traumatic Brain Injury: The Silent Epidemic

1992 ◽  
Vol 3 (1) ◽  
pp. 9-18 ◽  
Author(s):  
Kathy Coburn
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
National Database ◽  
Assessment Practices ◽  
Term Outcome ◽  
Long Term Outcome ◽  
Acute Health Care ◽  
Focal Injury ◽  
The Impact ◽  
The Brain

It is difficult to accurately determine the number of people affected annually by the devastating effects of traumatic brain injury. It is clear, however, that the impact of traumatic brain injury exceeds the financial cost of acute health care. The long-term outcome of patients with traumatic brain injury has been targeted specifically for improvement during this decade. The initial brain injury—known as the primary injury—may occur in one area of the brain (focal injury) or may affect the entire brain (diffuse injury). The outcome depends on many factors, including the severity of the brain injury and the effectiveness of the interventions received. Accurate assessment of the scope of the problem would be improved by the development of a national database and the standardization of assessment practices. Critical care nurses can contribute skill and knowledge in the care of patients with traumatic brain injury and in efforts to prevent the accidents and violence that cause traumatic brain injury

scholarly journals RhoA-ROCK Signaling as a Therapeutic Target in Traumatic Brain Injury

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 245 ◽  
Author(s):  
Shalaka Mulherkar ◽  
Kimberley F. Tolias
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Traumatic Event ◽  
Treatment Options ◽  
Work Productivity ◽  
Rho Kinase ◽  
Small Gtpase ◽  
Cns Injury ◽  
Functional Impairments ◽  
The Brain

Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. TBIs, which range in severity from mild to severe, occur when a traumatic event, such as a fall, a traffic accident, or a blow, causes the brain to move rapidly within the skull, resulting in damage. Long-term consequences of TBI can include motor and cognitive deficits and emotional disturbances that result in a reduced quality of life and work productivity. Recovery from TBI can be challenging due to a lack of effective treatment options for repairing TBI-induced neural damage and alleviating functional impairments. Central nervous system (CNS) injury and disease are known to induce the activation of the small GTPase RhoA and its downstream effector Rho kinase (ROCK). Activation of this signaling pathway promotes cell death and the retraction and loss of neural processes and synapses, which mediate information flow and storage in the brain. Thus, inhibiting RhoA-ROCK signaling has emerged as a promising approach for treating CNS disorders. In this review, we discuss targeting the RhoA-ROCK pathway as a therapeutic strategy for treating TBI and summarize the recent advances in the development of RhoA-ROCK inhibitors.

scholarly journals Can Therapeutic Hypothermia Diminish the Impact of Traumatic Brain Injury in Drosophila melanogaster?

2019 ◽  
Vol 13 ◽  
pp. 117906951882485 ◽  
Author(s):  
Shan Lateef ◽  
Aubrie Holman ◽  
Jessica Carpenter ◽  
Jennifer James
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Risk Ratio ◽  
Chronic Traumatic Encephalopathy ◽  
Survival Curve ◽  
Categorical Variables ◽  
Continuous Variables ◽  
The Impact ◽  
The Brain

Background/main objectives: No effective strategy exists to treat the well-recognized, devastating impact of traumatic brain injury (TBI) and chronic traumatic encephalopathy (CTE), which is the brain degeneration likely caused by repeated head trauma. The goals of this project were (1) to study the effects of single and recurrent TBI (rTBI) on Drosophila melanogaster’s (a) life span, (b) response to sedatives, and (c) behavioral responses to light and gravity and (2) to determine whether therapeutic hypothermia can mitigate the deleterious effects of TBI. Methods: Five experimental groups were created: (1) control, (2) single TBI or concussion; (3) concussion + hypothermia, (4) rTBI, and (5) rTBI + hypothermia. A “high-impact trauma” (HIT) device was built, which used a spring-based mechanism to propel flies against the wall of a vial, causing mechanical damage to the brain. Hypothermia groups were cooled to 15°C for 3 minutes. Group differences were analyzed with chi-square tests for the categorical variables and with ANOVA tests for the continuous variables. Results: Survival curve analysis showed that rTBI can decrease Drosophila lifespan and hypothermia diminished this impact. Average sedation time for control vs concussion vs concussion + hypothermia was 78 vs 52 vs 61 seconds ( P < .0001). Similarly, rTBI vs rTBI/hypothermia groups took 43 vs 59 seconds ( P < .0001). Concussed flies preferred dark environments compared with control flies (risk ratio 3.3, P < .01) while flies who were concussed and cooled had a risk ratio of 2.7 ( P < .01). Flies with rTBI were almost 4 times likely to prefer the dark environment but only 3 times as likely if they were cooled, compared with controls. Geotaxis was significantly affected by rTBI only and yet less so if rTBI flies were cooled. Conclusions: Hypothermia successfully mitigated many deleterious effects of single TBI and rTBI in Drosophila and may represent a promising breakthrough in the treatment of human TBI.

scholarly journals Apoptotic and Antiapoptotic Mechanisms after Traumatic Brain Injury

2001 ◽  
Vol 21 (10) ◽  
pp. 1189-1198 ◽  
Author(s):  
Robert W. Keane ◽  
Susan Kraydieh ◽  
George Lotocki ◽  
Ofelia F. Alonso ◽  
Phillip Aldana ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Protective Role ◽  
Current Data ◽  
Caspase 8 ◽  
Effector Caspase ◽  
Moderate Traumatic Brain Injury ◽  
Apoptotic Pathways ◽  
The Impact ◽  
The Brain

Caspase and inhibitor of apoptosis (IAP) expression was examined in rats subjected to moderate traumatic brain injury (TBI) using a parasagittal fluid-percussion brain insult (1.7 to 2.2 atm). Within 1 hour after injury, caspase-8 and −9, two initiators of apoptosis, were predominantly expressed in superficial cortical areas adjacent to the impact site and in the thalamus. Caspase-3, an effector caspase, was evident at 6 hours throughout the traumatized cerebral cortex and hippocampus. Moreover, the authors observed that XIAP, cIAP-1, and cIAP-2, members of the IAP family, were constitutively expressed in the brain. Colocalization of XIAP-immunolabled cells with cell-specific markers indicated that XIAP is expressed within neurons and a subpopulation of oligodendrocytes. Immunoblots of brain extracts revealed that the processed forms of caspase-8, −9, and −3 are present as early as 1 hour after trauma. The appearance of activated caspases corresponded with the detection of cleavage of XIAP into fragments after injury and a concomitant increase in the levels of cIAP-1 and cIAP-2 in the traumatized hemispheres. The current data are consistent with the hypotheses that caspases in both the extrinsic and intrinsic apoptotic pathways are activated after moderate TBI and that IAPs may have a protective role within the brain with alterations in levels and cleavage of IAPs that contribute to cell death in this setting.

scholarly journals Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Einars Kupats ◽  
Gundega Stelfa ◽  
Baiba Zvejniece ◽  
Solveiga Grinberga ◽  
Edijs Vavers ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Aminobutyric Acid ◽  
Drug Candidate ◽  
H2o2 Production ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
The Impact ◽  
The Brain

Altered neuronal Ca2+ homeostasis and mitochondrial dysfunction play a central role in the pathogenesis of traumatic brain injury (TBI). R-Phenibut ((3R)-phenyl-4-aminobutyric acid) is an antagonist of the α2δ subunit of voltage-dependent calcium channels (VDCC) and an agonist of gamma-aminobutyric acid B (GABA-B) receptors. The aim of this study was to evaluate the potential therapeutic effects of R-phenibut following the lateral fluid percussion injury (latFPI) model of TBI in mice and the impact of R- and S-phenibut on mitochondrial functionality in vitro. By determining the bioavailability of R-phenibut in the mouse brain tissue and plasma, we found that R-phenibut (50 mg/kg) reached the brain tissue 15 min after intraperitoneal (i.p.) and peroral (p.o.) injections. The maximal concentration of R-phenibut in the brain tissues was 0.6 μg/g and 0.2 μg/g tissue after i.p. and p.o. administration, respectively. Male Swiss-Webster mice received i.p. injections of R-phenibut at doses of 10 or 50 mg/kg 2 h after TBI and then once daily for 7 days. R-Phenibut treatment at the dose of 50 mg/kg significantly ameliorated functional deficits after TBI on postinjury days 1, 4, and 7. Seven days after TBI, the number of Nissl-stained dark neurons (N-DNs) and interleukin-1beta (IL-1β) expression in the cerebral neocortex in the area of cortical impact were reduced. Moreover, the addition of R- and S-phenibut at a concentration of 0.5 μg/ml inhibited calcium-induced mitochondrial swelling in the brain homogenate and prevented anoxia-reoxygenation-induced increases in mitochondrial H2O2 production and the H2O2/O ratio. Taken together, these results suggest that R-phenibut could serve as a neuroprotective agent and promising drug candidate for treating TBI.

A Study on the Impact of Helmet Padding Materials on the Brain Pressure Under Shock Loads

2012 ◽  
Author(s):  
Mehdi Salimi Jazi ◽  
Asghar Rezaei ◽  
Ghodrat Karami ◽  
Fardad Azarmi ◽  
Mariusz Ziejewski
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Motor Vehicle ◽  
Human Head ◽  
Motor Vehicle Crashes ◽  
Ballistic Impacts ◽  
Common Causes ◽  
The Impact ◽  
The Brain ◽  
Brain Pressure

A traumatic brain injury (TBI) can occur from a sharp strain, or acceleration, to the human head. Based on the level of injury, TBIs are classified as mild, moderate, or severe, with the most common causes being motor vehicle crashes; violence related injuries; collisions in sports; and falls are the most common causes of TBIs for the general public. Many soldiers experience a TBI in combat zones when they are exposed to the shock waves from blasts, or to ballistic impacts.

Lessons Learned From Coaching Postsecondary Students With Traumatic Brain Injury

2020 ◽  
Vol 5 (1) ◽  
pp. 88-96
Author(s):  
Mary R. T. Kennedy
Keyword(s):  
College Students ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Sense Of Self ◽  
Scientific Evidence ◽  
Sudden Onset ◽  
Lessons Learned ◽  
Speech Language Pathologists ◽  
The Brain ◽  
Exhaustive List

Purpose The purpose of this clinical focus article is to provide speech-language pathologists with a brief update of the evidence that provides possible explanations for our experiences while coaching college students with traumatic brain injury (TBI). Method The narrative text provides readers with lessons we learned as speech-language pathologists functioning as cognitive coaches to college students with TBI. This is not meant to be an exhaustive list, but rather to consider the recent scientific evidence that will help our understanding of how best to coach these college students. Conclusion Four lessons are described. Lesson 1 focuses on the value of self-reported responses to surveys, questionnaires, and interviews. Lesson 2 addresses the use of immediate/proximal goals as leverage for students to update their sense of self and how their abilities and disabilities may alter their more distal goals. Lesson 3 reminds us that teamwork is necessary to address the complex issues facing these students, which include their developmental stage, the sudden onset of trauma to the brain, and having to navigate going to college with a TBI. Lesson 4 focuses on the need for college students with TBI to learn how to self-advocate with instructors, family, and peers.

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