Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
Links | BibTeX | Tags: Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
keywords = {Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Ojo, J O; Mouzon, B C; Crawford, F
Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men Journal Article
In: Experimental Neurology, vol. 275, pp. 389–404, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends
@article{Ojo2016,
title = {Repetitive head trauma, chronic traumatic encephalopathy and tau: Challenges in translating from mice to men},
author = {Ojo, J O and Mouzon, B C and Crawford, F},
doi = {10.1016/j.expneurol.2015.06.003},
year = {2016},
date = {2016-01-01},
journal = {Experimental Neurology},
volume = {275},
pages = {389--404},
abstract = {Chronic traumatic encephalopathy (CTE) is a neurological and psychiatric condition marked by preferential perivascular foci of neurofibrillary and glial tangles (composed of hyperphosphorylated-tau proteins) in the depths of the sulci. Recent retrospective case series published over the last decade on athletes and military personnel have added considerably to our clinical and histopathological knowledge of CTE. This has marked a vital turning point in the traumatic brain injury (TBI) field, raising public awareness of the potential long-term effects of mild and moderate repetitive TBI, which has been recognized as one of the major risk factors associated with CTE. Although these human studies have been informative, their retrospective design carries certain inherent limitations that should be cautiously interpreted. In particular, the current overriding issue in the CTE literature remains confusing in regard to appropriate definitions of terminology, variability in individual pathologies and the potential case selection bias in autopsy based studies. There are currently no epidemiological or prospective studies on CTE. Controlled preclinical studies in animals therefore provide an alternative means for specifically interrogating aspects of CTE pathogenesis. In this article, we review the current literature and discuss difficulties and challenges of developing in-vivo TBI experimental paradigms to explore the link between repetitive head trauma and tau-dependent changes. We provide our current opinion list of recommended features to consider for successfully modeling CTE in animals to better understand the pathobiology and develop therapeutics and diagnostics, and critical factors, which might influence outcome. We finally discuss the possible directions of future experimental research in the repetitive TBI/CTE field. © 2015 Elsevier Inc..},
keywords = {amyloid beta protein, animal, Animal models, Animals, Astroglial tangles, Brain Injury, cell activation, Chronic, complication, Concussion, Craniocerebral Trauma, CTE, diffuse axonal injury, disease duration, disease model, Disease Models, genetic predisposition, gliosis, head injury, hippocampus, human, Humans, lifestyle modification, lithium, metabolism, Mice, microglia, minocycline, mouse, nervous system inflammation, Neurobehaviour, Neurofibrillary tangles, neuropathology, nonhuman, pathogenesis, pathology, priority journal, procedures, protein aggregation, protein analysis, protein blood level, protein cleavage, Repetitive TBI, Review, sex difference, stress activated protein kinase inhibitor, Systematic Review, Tau, tau protein, tau Proteins, Transgenic mice, Translational Medical Research, translational research, traumatic brain injury, trends},
pubstate = {published},
tppubtype = {article}
}
Moon, K; Theodore, N
Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists? Journal Article
In: World Neurosurgery, vol. 89, pp. 720–721, 2016.
Links | BibTeX | Tags: Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury
@article{Moon2016,
title = {Football and Chronic Traumatic Encephalopathy: How Much Evidence Actually Exists?},
author = {Moon, K and Theodore, N},
doi = {10.1016/j.wneu.2016.03.073},
year = {2016},
date = {2016-01-01},
journal = {World Neurosurgery},
volume = {89},
pages = {720--721},
keywords = {Alzheimer disease, amyloid beta protein, amyloid plaque, anxiety disorder, apolipoprotein E, Article, behavior disorder, Boxing, brain atrophy, brain concussion, brain degeneration, chronic disease, Chronic traumatic encephalopathy, cognitive defect, degenerative disease, depression, environmental factor, football, frontotemporal dementia, genetic predisposition, genetic risk, genetic susceptibility, human, motor control, Neuroanatomy, opiate addiction, Parkinson disease, protein phosphorylation, scar formation, septum pellucidum, sport injury, substantia nigra, suicide, TAR DNA binding protein, tau protein, tauopathy, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Lawrence, D W; Comper, P; Hutchison, M G; Sharma, B
The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review Journal Article
In: Brain Injury, vol. 29, no. 9, pp. 1018–1031, 2015.
Abstract | Links | BibTeX | Tags: 80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale
@article{Lawrence2015,
title = {The role of apolipoprotein E episilon ($epsilon$)-4 allele on outcome following traumatic brain injury: A systematic review},
author = {Lawrence, D W and Comper, P and Hutchison, M G and Sharma, B},
doi = {10.3109/02699052.2015.1005131},
year = {2015},
date = {2015-01-01},
journal = {Brain Injury},
volume = {29},
number = {9},
pages = {1018--1031},
abstract = {Background: The apolipoprotein E gene (APOE) has emerged as a candidate for prognosticating traumatic brain injury (TBI) recovery, with APOE$epsilon$4 identified as a susceptibility marker for poor outcome, despite large discrepancy in its reported influence post-TBI.Methods: A systematic review was conducted, including all primary articles investigating the role of APOE$epsilon$4 on TBI outcome. A total of 65 studies were included, including 24 predominantly investigating mild (mTBI), seven moderate (modTBI) and 33 severe (sTBI); severity was not reported in one study.Results: In mTBI studies, the association between APOE$epsilon$4 and post-TBI outcome was concluded as non-contributory in 14 studies (58.3%), hazardous in nine (37.5%) and protective in one (4.2%). In sTBI studies, the role of APOE$epsilon$4 was hazardous in 21 (63.6%), non-contributory in nine (27.3%) and protective in three (9.1%). Of the seven studies investigating dementia outcomes, four observed a hazardous association with APOE$epsilon$4, while three reported no association. Six studies examined Alzheimers dementia pathology, of which three reported a hazardous influence of APOE$epsilon$4.Conclusions: The influence of APOE$epsilon$4 on neuropsychological testing, functional outcome and in paediatric populations was incongruous. This review supports the majority of research indicating APOE$epsilon$4 adversely influences recovery following TBI, particularly with respect to dementia-related outcomes and outcomes following sTBI. © 2015 Taylor \& Francis Group, LLC.},
keywords = {80 and over, aged, allele, Alleles, Alzheimer disease, amyloid beta protein, APOE, apolipoprotein E, apolipoprotein E4, Article, athlete, brain concussion, Brain Injuries, clinical evaluation, cognition, cognitive defect, disease severity, Female, follow up, genetic association, genetic risk, genetics, GENOTYPE, Glasgow Outcome Scale, heterozygote, histopathology, homozygote, human, Humans, Incidence, injury severity, Male, Memory, nerve cell necrosis, neuropathology, Neuroprotection, outcome assessment, pediatrics, Prevalence, Prognosis, prognostic assessment, protein function, psychologic test, psychology, Recovery, scoring system, Systematic Review, tau protein, traumatic brain injury, treatment outcome, very elderly, Wechsler Intelligence Scale},
pubstate = {published},
tppubtype = {article}
}