Lucke-Wold, B P; Naser, Z J; Logsdon, A F; Turner, R C; Smith, K E; Robson, M J; Bailes, J E; Lee, J M; Rosen, C L; Huber, J D
Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury Journal Article
In: Translational Research: The Journal Of Laboratory & Clinical Medicine, vol. 166, no. 6, pp. 509–528.e1, 2015.
Abstract | BibTeX | Tags: *Blast Injuries/pa [Pathology], *Brain Injuries/pa [Pathology], *NADPH Oxidase/me [Metabolism], *Oxidative Stress, 73Y7P0K73Y (Thioctic Acid), Animals, Apoptosis, Blast Injuries/en [Enzymology], Blast Injuries/me [Metabolism], Brain Injuries/en [Enzymology], Brain Injuries/me [Metabolism], EC 1-6-3-1 (NADPH Oxidase), Male, Rats, Sprague-Dawley, Thioctic Acid/pd [Pharmacology]
@article{Lucke-Wold2015,
title = {Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury},
author = {Lucke-Wold, B P and Naser, Z J and Logsdon, A F and Turner, R C and Smith, K E and Robson, M J and Bailes, J E and Lee, J M and Rosen, C L and Huber, J D},
year = {2015},
date = {2015-01-01},
journal = {Translational Research: The Journal Of Laboratory \& Clinical Medicine},
volume = {166},
number = {6},
pages = {509--528.e1},
abstract = {A total of 1.7 million traumatic brain injuries (TBIs) occur each year in the United States, but available pharmacologic options for the treatment of acute neurotrauma are limited. Oxidative stress is an important secondary mechanism of injury that can lead to neuronal apoptosis and subsequent behavioral changes. Using a clinically relevant and validated rodent blast model, we investigated how nicotinamide adenine dinucleotide phosphate oxidase (Nox) expression and associated oxidative stress contribute to cellular apoptosis after single and repeat blast injuries. Nox4 forms a complex with p22phox after injury, forming free radicals at neuronal membranes. Using immunohistochemical-staining methods, we found a visible increase in Nox4 after single blast injury in Sprague Dawley rats. Interestingly, Nox4 was also increased in postmortem human samples obtained from athletes diagnosed with chronic traumatic encephalopathy. Nox4 activity correlated with an increase in superoxide formation. Alpha-lipoic acid, an oxidative stress inhibitor, prevented the development of superoxide acutely and increased antiapoptotic markers B-cell lymphoma 2 (t = 3.079, P \< 0.05) and heme oxygenase 1 (t = 8.169, P \< 0.001) after single blast. Subacutely, alpha-lipoic acid treatment reduced proapoptotic markers Bax (t = 4.483, P \< 0.05), caspase 12 (t = 6.157, P \< 0.001), and caspase 3 (t = 4.573, P \< 0.01) after repetitive blast, and reduced tau hyperphosphorylation indicated by decreased CP-13 and paired helical filament staining. Alpha-lipoic acid ameliorated impulsive-like behavior 7 days after repetitive blast injury (t = 3.573, P \< 0.05) compared with blast exposed animals without treatment. TBI can cause debilitating symptoms and psychiatric disorders. Oxidative stress is an ideal target for neuropharmacologic intervention, and alpha-lipoic acid warrants further investigation as a therapeutic for prevention of chronic neurodegeneration. Copyright © 2015 Elsevier Inc. All rights reserved.},
keywords = {*Blast Injuries/pa [Pathology], *Brain Injuries/pa [Pathology], *NADPH Oxidase/me [Metabolism], *Oxidative Stress, 73Y7P0K73Y (Thioctic Acid), Animals, Apoptosis, Blast Injuries/en [Enzymology], Blast Injuries/me [Metabolism], Brain Injuries/en [Enzymology], Brain Injuries/me [Metabolism], EC 1-6-3-1 (NADPH Oxidase), Male, Rats, Sprague-Dawley, Thioctic Acid/pd [Pharmacology]},
pubstate = {published},
tppubtype = {article}
}
Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
Abstract | Links | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
Abstract | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds},
pubstate = {published},
tppubtype = {article}
}
Lucke-Wold, B P; Naser, Z J; Logsdon, A F; Turner, R C; Smith, K E; Robson, M J; Bailes, J E; Lee, J M; Rosen, C L; Huber, J D
Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury Journal Article
In: Translational Research: The Journal Of Laboratory & Clinical Medicine, vol. 166, no. 6, pp. 509–528.e1, 2015.
@article{Lucke-Wold2015,
title = {Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury},
author = {Lucke-Wold, B P and Naser, Z J and Logsdon, A F and Turner, R C and Smith, K E and Robson, M J and Bailes, J E and Lee, J M and Rosen, C L and Huber, J D},
year = {2015},
date = {2015-01-01},
journal = {Translational Research: The Journal Of Laboratory \& Clinical Medicine},
volume = {166},
number = {6},
pages = {509--528.e1},
abstract = {A total of 1.7 million traumatic brain injuries (TBIs) occur each year in the United States, but available pharmacologic options for the treatment of acute neurotrauma are limited. Oxidative stress is an important secondary mechanism of injury that can lead to neuronal apoptosis and subsequent behavioral changes. Using a clinically relevant and validated rodent blast model, we investigated how nicotinamide adenine dinucleotide phosphate oxidase (Nox) expression and associated oxidative stress contribute to cellular apoptosis after single and repeat blast injuries. Nox4 forms a complex with p22phox after injury, forming free radicals at neuronal membranes. Using immunohistochemical-staining methods, we found a visible increase in Nox4 after single blast injury in Sprague Dawley rats. Interestingly, Nox4 was also increased in postmortem human samples obtained from athletes diagnosed with chronic traumatic encephalopathy. Nox4 activity correlated with an increase in superoxide formation. Alpha-lipoic acid, an oxidative stress inhibitor, prevented the development of superoxide acutely and increased antiapoptotic markers B-cell lymphoma 2 (t = 3.079, P \< 0.05) and heme oxygenase 1 (t = 8.169, P \< 0.001) after single blast. Subacutely, alpha-lipoic acid treatment reduced proapoptotic markers Bax (t = 4.483, P \< 0.05), caspase 12 (t = 6.157, P \< 0.001), and caspase 3 (t = 4.573, P \< 0.01) after repetitive blast, and reduced tau hyperphosphorylation indicated by decreased CP-13 and paired helical filament staining. Alpha-lipoic acid ameliorated impulsive-like behavior 7 days after repetitive blast injury (t = 3.573, P \< 0.05) compared with blast exposed animals without treatment. TBI can cause debilitating symptoms and psychiatric disorders. Oxidative stress is an ideal target for neuropharmacologic intervention, and alpha-lipoic acid warrants further investigation as a therapeutic for prevention of chronic neurodegeneration. Copyright © 2015 Elsevier Inc. All rights reserved.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Lucke-Wold, B P; Naser, Z J; Logsdon, A F; Turner, R C; Smith, K E; Robson, M J; Bailes, J E; Lee, J M; Rosen, C L; Huber, J D
Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury Journal Article
In: Translational Research: The Journal Of Laboratory & Clinical Medicine, vol. 166, no. 6, pp. 509–528.e1, 2015.
Abstract | BibTeX | Tags: *Blast Injuries/pa [Pathology], *Brain Injuries/pa [Pathology], *NADPH Oxidase/me [Metabolism], *Oxidative Stress, 73Y7P0K73Y (Thioctic Acid), Animals, Apoptosis, Blast Injuries/en [Enzymology], Blast Injuries/me [Metabolism], Brain Injuries/en [Enzymology], Brain Injuries/me [Metabolism], EC 1-6-3-1 (NADPH Oxidase), Male, Rats, Sprague-Dawley, Thioctic Acid/pd [Pharmacology]
@article{Lucke-Wold2015,
title = {Amelioration of nicotinamide adenine dinucleotide phosphate-oxidase mediated stress reduces cell death after blast-induced traumatic brain injury},
author = {Lucke-Wold, B P and Naser, Z J and Logsdon, A F and Turner, R C and Smith, K E and Robson, M J and Bailes, J E and Lee, J M and Rosen, C L and Huber, J D},
year = {2015},
date = {2015-01-01},
journal = {Translational Research: The Journal Of Laboratory \& Clinical Medicine},
volume = {166},
number = {6},
pages = {509--528.e1},
abstract = {A total of 1.7 million traumatic brain injuries (TBIs) occur each year in the United States, but available pharmacologic options for the treatment of acute neurotrauma are limited. Oxidative stress is an important secondary mechanism of injury that can lead to neuronal apoptosis and subsequent behavioral changes. Using a clinically relevant and validated rodent blast model, we investigated how nicotinamide adenine dinucleotide phosphate oxidase (Nox) expression and associated oxidative stress contribute to cellular apoptosis after single and repeat blast injuries. Nox4 forms a complex with p22phox after injury, forming free radicals at neuronal membranes. Using immunohistochemical-staining methods, we found a visible increase in Nox4 after single blast injury in Sprague Dawley rats. Interestingly, Nox4 was also increased in postmortem human samples obtained from athletes diagnosed with chronic traumatic encephalopathy. Nox4 activity correlated with an increase in superoxide formation. Alpha-lipoic acid, an oxidative stress inhibitor, prevented the development of superoxide acutely and increased antiapoptotic markers B-cell lymphoma 2 (t = 3.079, P \< 0.05) and heme oxygenase 1 (t = 8.169, P \< 0.001) after single blast. Subacutely, alpha-lipoic acid treatment reduced proapoptotic markers Bax (t = 4.483, P \< 0.05), caspase 12 (t = 6.157, P \< 0.001), and caspase 3 (t = 4.573, P \< 0.01) after repetitive blast, and reduced tau hyperphosphorylation indicated by decreased CP-13 and paired helical filament staining. Alpha-lipoic acid ameliorated impulsive-like behavior 7 days after repetitive blast injury (t = 3.573, P \< 0.05) compared with blast exposed animals without treatment. TBI can cause debilitating symptoms and psychiatric disorders. Oxidative stress is an ideal target for neuropharmacologic intervention, and alpha-lipoic acid warrants further investigation as a therapeutic for prevention of chronic neurodegeneration. Copyright © 2015 Elsevier Inc. All rights reserved.},
keywords = {*Blast Injuries/pa [Pathology], *Brain Injuries/pa [Pathology], *NADPH Oxidase/me [Metabolism], *Oxidative Stress, 73Y7P0K73Y (Thioctic Acid), Animals, Apoptosis, Blast Injuries/en [Enzymology], Blast Injuries/me [Metabolism], Brain Injuries/en [Enzymology], Brain Injuries/me [Metabolism], EC 1-6-3-1 (NADPH Oxidase), Male, Rats, Sprague-Dawley, Thioctic Acid/pd [Pharmacology]},
pubstate = {published},
tppubtype = {article}
}
Omalu, B
Chronic traumatic encephalopathy Journal Article
In: Progress in Neurological Surgery, vol. 28, pp. 38–49, 2014.
Abstract | Links | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies
@article{Omalu2014,
title = {Chronic traumatic encephalopathy},
author = {Omalu, B},
url = {http://ovidsp.ovid.com/ovidweb.cgi?T=JS\&CSC=Y\&NEWS=N\&PAGE=fulltext\&D=medl\&AN=24923391},
year = {2014},
date = {2014-01-01},
journal = {Progress in Neurological Surgery},
volume = {28},
pages = {38--49},
abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative syndrome, which is caused by single, episodic, or repetitive blunt force impacts to the head and transfer of acceleration-deceleration forces to the brain. CTE presents clinically as a composite syndrome of mood disorders and behavioral and cognitive impairment, with or without sensorimotor impairment. Symptoms of CTE may begin with persistent symptoms of acute traumatic brain injury (TBI) following a documented episode of brain trauma or after a latent period that may range from days to weeks to months and years, up to 40 years following a documented episode of brain trauma or cessation of repetitive TBI. Posttraumatic encephalopathy is distinct from CTE, can be comorbid with CTE, and is a clinicopathologic syndrome induced by focal and/or diffuse, gross and/or microscopic destruction of brain tissue following brain trauma. The brain of a CTE sufferer may appear grossly unremarkable, but shows microscopic evidence of primary and secondary proteinopathies. The primary proteinopathy of CTE is tauopathy, while secondary proteinopathies may include, but are not limited to, amyloidopathy and TDP proteinopathy. Reported prevalence rates of CTE in cohorts exposed to TBI ranges from 3 to 80% across age groups.Copyright © 2014 S. Karger AG, Basel.},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injury, Brain Concussion/pa [Pathology], Chronic Traumatic Encephalopathy Animals, Chronic/pa [Pathology], Humans, Tauopathies},
pubstate = {published},
tppubtype = {article}
}
Davis, A E
Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations Journal Article
In: Critical Care Nursing Quarterly, vol. 23, no. 3, pp. 1–13, 2000.
Abstract | BibTeX | Tags: *Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds
@article{Davis2000,
title = {Mechanisms of traumatic brain injury: biomechanical, structural and cellular considerations},
author = {Davis, A E},
year = {2000},
date = {2000-01-01},
journal = {Critical Care Nursing Quarterly},
volume = {23},
number = {3},
pages = {1--13},
abstract = {Traumatic brain injury (TBI) is a public health problem of great concern, because it affects more than 2 million individuals each year. TBI occurs as a result of motor vehicle crashes, falls, and sports-related events. Biomechanical mechanisms occurring at the time of the injury initiate primary and secondary injuries that evolve over several days. In this article the relationship between an blunt injury event and the subsequent damage produced is addressed. Mechanisms of brain injury from biomechanics to cellular pathobiology are presented. Primary and secondary injuries are differentiated, and specific focal and diffuse clinical syndromes are described. Cellular mechanisms responsible for injury are also addressed, because they provide the unifying concepts across the many clinical syndromes so often discussed separately in reviews of traumatic brain injury. [References: 26]},
keywords = {*Brain Injuries/pa [Pathology], *Brain Injuries/pp [Physiopathology], Biomechanical Phenomena, Brain Injuries/cl [Classification], Brain Injuries/co [Complications], Brain/me [Metabolism], Brain/pa [Pathology], Humans, intracranial hemorrhage, Neurons/me [Metabolism], Neurons/pa [Pathology], Nonpenetrating/pa [Pathology], Nonpenetrating/pp [Physiopathology], Skull Fractures/pa [Pathology], Skull Fractures/pp [Physiopathology], Traumatic/pa [Pathology], Traumatic/pp [Physiopatho, Wounds},
pubstate = {published},
tppubtype = {article}
}