Traumatic brain injury and repetitive brain trauma: Chronic traumatic encephalopathy and dementia syndromes.

2018 ◽  
pp. 67-84
Author(s):  
Breton M. Asken ◽  
Russell M. Bauer
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Brain Trauma ◽  
Repetitive Brain Trauma

scholarly journals The Correlation between Administration of Alpha Lipoic Acid and Malondialdehyde Level on Traumatic Brain Injury Model Rat’s Brain

2018 ◽  
Vol 4 (1) ◽  
pp. 31
Author(s):  
Nastiti Bekti Utami ◽  
Dini Agustina ◽  
Erfan Efendi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Effective Dose ◽  
Lipoic Acid ◽  
Chronic Traumatic Encephalopathy ◽  
Alpha Lipoic Acid ◽  
Injury Model ◽  
Neuron Damage ◽  
Injury Treatment ◽  
Repetitive Brain Trauma

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive brain trauma that cancontinues to be dementia, alzheimer and parkinsonism. Traumatic brain injury increased free radicals in brain thatcaused oxidative stress and induced lipid peroxidation, neuron damage and producing MDA. The purpose is todetermine the correlation between administration of ALA and MDA level in rat’s brain model of traumatic braininjury and its effective dose. Rats are randomLy divided into 7 groups. Normal group without treatment, K(-) wasgiven NaCl 0,9% 1,5 mL, K(+) was given citicoline 6,75 mg, K1 was given ALA 1,0125 mg, K2 was given ALA 2,025mg, K3 was given ALA 4,05 mg, K4 was given ALA 8,1 mg and received 30 days traumatic brain injury treatment bydropped 245 g load on the rat’s head at 35 cm height. MDA level in brain were measured on the 31th day withMDA-TBA method by spectrofotometer. The averages of MDA levels were N 1,64 μg/mL; K(+) 2,09 μg/mL; K(-) 4,87μg/mL; K1 2,73 μg/mL; K2 2,68 μg/mL; K3 2,20 μg/mL and K4 2,02 μg/mL. Pearson’s analysis shows strong andsignificant negative correlation (r= -0,790) between administration of ALA and MDA level in rat’s brain model oftraumatic brain injury (p<0,05). The effective dose of ALA is 8,625 mg/150gBW.Keywords : Alpha lipoic acid, MDA, traumatic brain injury, CTE

scholarly journals Pathologically Entangled: Brain trauma-evoked ROS imbalance disrupts Kir channel function in distant peripheral vessels

Function ◽  
2021 ◽  
Author(s):  
Nick Weir ◽  
Thomas A Longden
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Potassium Channels ◽  
Vascular Function ◽  
Inward Rectifier ◽  
Brain Trauma ◽  
Channel Function ◽  
Inward Rectifier Potassium Channels ◽  
Kir Channel

Abstract A Perspective on "Traumatic Brain Injury Impairs Systemic Vascular Function Through Disruption of Inward-Rectifier Potassium Channels"

scholarly journals Unconventional animal models for traumatic brain injury and chronic traumatic encephalopathy

2021 ◽  
Author(s):  
Nicole L. Ackermans ◽  
Merina Varghese ◽  
Bridget Wicinski ◽  
Joshua Torres ◽  
Rita De Gasperi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Animal Models ◽  
Chronic Traumatic Encephalopathy

Blood biomarkers for assessment of mild traumatic brain injury and chronic traumatic encephalopathy

Biomarkers ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 213-227 ◽  
Author(s):  
Matthew I. Hiskens ◽  
Anthony G. Schneiders ◽  
Mariana Angoa-Pérez ◽  
Rebecca K. Vella ◽  
Andrew S. Fenning
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Chronic Traumatic Encephalopathy ◽  
Blood Biomarkers

Levetiracetam Treatment in Traumatic Brain Injury: Operation Brain Trauma Therapy

2016 ◽  
Vol 33 (6) ◽  
pp. 581-594 ◽  
Author(s):  
Megan Browning ◽  
Deborah A. Shear ◽  
Helen M. Bramlett ◽  
C. Edward Dixon ◽  
Stefania Mondello ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Trauma ◽  
Trauma Therapy

Serum-Based Phospho-Neurofilament-Heavy Protein as Theranostic Biomarker in Three Models of Traumatic Brain Injury: An Operation Brain Trauma Therapy Study

2019 ◽  
Vol 36 (2) ◽  
pp. 348-359 ◽  
Author(s):  
Zhihui Yang ◽  
Tian Zhu ◽  
Stefania Mondello ◽  
Miis Akel ◽  
Aaron T. Wong ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Trauma ◽  
Trauma Therapy

The Role of Inflammation in Traumatic Brain Injury

Neurotrauma ◽  
2018 ◽  
pp. 211-232
Author(s):  
Sarah C. Hellewell ◽  
Bridgette D. Semple ◽  
Jenna M. Ziebell ◽  
Nicole Bye ◽  
Cristina Morganti-Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Cells ◽  
Immune Cell ◽  
Brain Trauma ◽  
Multiple Roles ◽  
Cell Functions ◽  
Macrophage Populations

Inflammation occurring following brain trauma represents a significant constituent of complex secondary responses that dictate patients’ outcome. Although a few decades have passed since its discovery, new aspects of this intriguing phenomenon are still being uncovered, ranging from the multiple roles of mediators regulating the inception, progression, and resolution of neuroinflammation, to the development of antiinflammatory therapies. This review provides a summary of the vast research on traumatic brain injury inflammation. The authors describe the fundamental aspects of cytokine and immune cell functions, the orchestrated collaboration of chemokines and leukocytes, the phenotypic distinction of macrophage populations, and the contribution of glial cells. Among the beneficial properties of neuroinflammation, they briefly discuss cytokines’ impact on neurogenesis; the chapter concludes by touching on the implications of antiinflammatory therapies.

scholarly journals Xenon treatment after severe traumatic brain injury improves locomotor outcome, reduces acute neuronal loss and enhances early beneficial neuroinflammation: a randomized, blinded, controlled animal study

Critical Care ◽  
2020 ◽  
Vol 24 (1) ◽  
Author(s):  
Rita Campos-Pires ◽  
Haldis Onggradito ◽  
Eszter Ujvari ◽  
Shughoofa Karimi ◽  
Flavia Valeo ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
Brain Trauma ◽  
Lesion Volume ◽  
Oxygen Balance ◽  
Sprague Dawley ◽  
Locomotor Deficits

Abstract Background Traumatic brain injury (TBI) is a major cause of morbidity and mortality, but there are no clinically proven treatments that specifically target neuronal loss and secondary injury development following TBI. In this study, we evaluate the effect of xenon treatment on functional outcome, lesion volume, neuronal loss and neuroinflammation after severe TBI in rats. Methods Young adult male Sprague Dawley rats were subjected to controlled cortical impact (CCI) brain trauma or sham surgery followed by treatment with either 50% xenon:25% oxygen balance nitrogen, or control gas 75% nitrogen:25% oxygen. Locomotor function was assessed using Catwalk-XT automated gait analysis at baseline and 24 h after injury. Histological outcomes were assessed following perfusion fixation at 15 min or 24 h after injury or sham procedure. Results Xenon treatment reduced lesion volume, reduced early locomotor deficits, and attenuated neuronal loss in clinically relevant cortical and subcortical areas. Xenon treatment resulted in significant increases in Iba1-positive microglia and GFAP-positive reactive astrocytes that was associated with neuronal preservation. Conclusions Our findings demonstrate that xenon improves functional outcome and reduces neuronal loss after brain trauma in rats. Neuronal preservation was associated with a xenon-induced enhancement of microglial cell numbers and astrocyte activation, consistent with a role for early beneficial neuroinflammation in xenon’s neuroprotective effect. These findings suggest that xenon may be a first-line clinical treatment for brain trauma.

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