References

2016

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

2015

Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C

Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article

In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.

Abstract | Links | BibTeX | Tags: A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds & injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds & injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury

@article{Daneshvar2015,

title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},

author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},

url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},

doi = {10.1016/j.mcn.2015.03.007},

isbn = {10447431},

year  = {2015},

date = {2015-01-01},

journal = {MCN: Molecular \& Cellular Neuroscience},

volume = {66},

number = {Part B},

pages = {81--90},

abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},

keywords = {A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds \&amp; injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds \&amp; injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, traumatic brain injury},

pubstate = {published},

tppubtype = {article}

}

Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables—including age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities—all of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular & Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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}

}

2014

Stein, T D; Alvarez, V E; McKee, A C

Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article

In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.

Abstract | Links | BibTeX | Tags: Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran

@article{Stein2014,

title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},

author = {Stein, T D and Alvarez, V E and McKee, A C},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},

doi = {10.1186/alzrt234},

year  = {2014},

date = {2014-01-01},

journal = {Alzheimer's Research and Therapy},

volume = {6},

number = {1},

abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},

keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},

pubstate = {published},

tppubtype = {article}

}

Ling, H; Kara, E; Revesz, T; Lees, A J; Plant, G T; Martino, D; Houlden, H; Hardy, J; Holton, J L

Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer Journal Article

In: Acta neuropathologica communications, vol. 2, pp. 24, 2014.

Abstract | Links | BibTeX | Tags: aged, Brain Injury, case report, Chronic, Chronic Traumatic Encephalopathy GRN protein, complication, genetics, huma, human, Humans, Intercellular Signaling Peptides and Proteins, LRRK2 protein, Male, MAPT protein, pathology, Progressive, progressive supranuclear palsy, protein serine threonine kinase, Protein-Serine-Threonine Kinases, signal peptide, Supranuclear Palsy, tau protein, tau Proteins

Reference Search

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

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

@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.

Links | BibTeX

Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C

Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article

In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.

Abstract | Links | BibTeX

@article{Daneshvar2015,

title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},

author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},

url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},

doi = {10.1016/j.mcn.2015.03.007},

isbn = {10447431},

year  = {2015},

date = {2015-01-01},

journal = {MCN: Molecular \& Cellular Neuroscience},

volume = {66},

number = {Part B},

pages = {81--90},

abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},

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.

Abstract | Links | BibTeX

@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}

}

Stein, T D; Alvarez, V E; McKee, A C

Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article

In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.

Abstract | Links | BibTeX

@article{Stein2014,

title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},

author = {Stein, T D and Alvarez, V E and McKee, A C},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},

doi = {10.1186/alzrt234},

year  = {2014},

date = {2014-01-01},

journal = {Alzheimer's Research and Therapy},

volume = {6},

number = {1},

abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

Ling, H; Kara, E; Revesz, T; Lees, A J; Plant, G T; Martino, D; Houlden, H; Hardy, J; Holton, J L

Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer Journal Article

In: Acta neuropathologica communications, vol. 2, pp. 24, 2014.

Abstract | Links | BibTeX

Most Referenced Keywords

Show all

2016

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 = {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.

@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.

2015

Daneshvar, Daniel H; Goldstein, Lee E; Kiernan, Patrick T; Stein, Thor D; McKee, Ann C

Post-traumatic neurodegeneration and chronic traumatic encephalopathy Journal Article

In: MCN: Molecular & Cellular Neuroscience, vol. 66, no. Part B, pp. 81–90, 2015, ISBN: 10447431.

@article{Daneshvar2015,

title = {Post-traumatic neurodegeneration and chronic traumatic encephalopathy},

author = {Daneshvar, Daniel H and Goldstein, Lee E and Kiernan, Patrick T and Stein, Thor D and McKee, Ann C},

url = {http://search.ebscohost.com/login.aspx?direct=true\&db=aph\&AN=103136351\&site=ehost-live},

doi = {10.1016/j.mcn.2015.03.007},

isbn = {10447431},

year  = {2015},

date = {2015-01-01},

journal = {MCN: Molecular \& Cellular Neuroscience},

volume = {66},

number = {Part B},

pages = {81--90},

abstract = {Traumatic brain injury (TBI) is a leading cause of mortality and morbidity around the world. Concussive and subconcussive forms of closed-head injury due to impact or blast neurotrauma represent the most common types of TBI in civilian and military settings. It is becoming increasingly evident that TBI can lead to persistent, long-term debilitating effects, and in some cases, progressive neurodegeneration and chronic traumatic encephalopathy (CTE). The epidemiological literature suggests that a single moderate-to-severe TBI may be associated with accelerated neurodegeneration and increased risk of Alzheimer's disease, Parkinson's disease, or motor neuron disease. However, the pathologic phenotype of these post-traumatic neurodegenerations is largely unknown and there may be pathobiological differences between post-traumatic disease and the corresponding sporadic disorder. By contrast, the pathology of CTE is increasingly well known and is characterized by a distinctive pattern of progressive brain atrophy and accumulation of hyperphosphorylated tau neurofibrillary and glial tangles, dystrophic neurites, 43 kDa TAR DNA-binding protein (TDP-43) neuronal and glial aggregates, microvasculopathy, myelinated axonopathy, neuroinflammation, and white matter degeneration. Clinically, CTE is associated with behavioral changes, executive dysfunction, memory deficits, and cognitive impairments that begin insidiously and most often progress slowly over decades. Although research on the long-term effects of TBI is advancing quickly, the incidence and prevalence of post-traumatic neurodegeneration and CTE are unknown. Critical knowledge gaps include elucidation of pathogenic mechanisms, identification of genetic risk factors, and clarification of relevant variables\textemdashincluding age at exposure to trauma, history of prior and subsequent head trauma, substance use, gender, stress, and comorbidities\textemdashall of which may contribute to risk profiles and the development of post-traumatic neurodegeneration and CTE. This article is part of a Special Issue entitled 'Traumatic Brain Injury'. [ABSTRACT FROM AUTHOR] Copyright of MCN: Molecular \& Cellular Neuroscience is the property of Academic Press Inc. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)},

keywords = {A$beta$ beta-amyloid, AD Alzheimer's disease, APOE $epsilon$4 apolipoprotein $epsilon$4, axonal injury, Blast and impact neurotrauma, BRAIN -- Wounds \&amp; injuries, Brain trauma, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy NEURODEGENERATION, Concussion, CSF cerebrospinal fluid, CTE chronic traumatic encephalopathy, DIAGNOSIS, DISEASES -- Risk factors, DNA-binding proteins, MORTALITY, Motor neuron disease, mTBI mild traumatic brain injury, NERVOUS system -- Wounds \&amp; injuries, NFTs neurofibrillary tangles, p-tau hyperphosphorylated tau, PCS post-concussion syndrome, PET positron emission tomography, PHF-tau paired helical filament-tau, Posttraumatic neurodegeneration, tau protein, TBI traumatic brain injury, TDP-43 43 kDa TAR DNA-binding protein, 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.

@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}

}

2014

Stein, T D; Alvarez, V E; McKee, A C

Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel Journal Article

In: Alzheimer's Research and Therapy, vol. 6, no. 1, 2014.

@article{Stein2014,

title = {Chronic traumatic encephalopathy: A spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel},

author = {Stein, T D and Alvarez, V E and McKee, A C},

url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84892718392\&partnerID=40\&md5=c39a0e58ad33cee7a570b4681131d6ea},

doi = {10.1186/alzrt234},

year  = {2014},

date = {2014-01-01},

journal = {Alzheimer's Research and Therapy},

volume = {6},

number = {1},

abstract = {Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (\>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined. © 2014 BioMed Central Ltd.},

keywords = {Aggression, Alzheimer disease, amnesia, army, astrocyte, athlete, behavior change, brain atrophy, brain stem, brain weight, central sulcus, chronic disease, Chronic Traumatic Encephalopathy TAR DNA binding p, cognitive defect, comorbidity, Dementia, depression, diencephalon, diffuse Lewy body disease, exposure, frontotemporal dementia, human, impulsiveness, irritability, Motor neuron disease, nerve fiber, neurite, neurofibrillary tangle, neuropathology, nonhuman, personality disorder, priority journal, Review, short term memory, soldier, staging, suicidal ideation, tau protein, tauopathy, temporal lobe, traumatic brain injury, veteran},

pubstate = {published},

tppubtype = {article}

}

Ling, H; Kara, E; Revesz, T; Lees, A J; Plant, G T; Martino, D; Houlden, H; Hardy, J; Holton, J L

Concomitant progressive supranuclear palsy and chronic traumatic encephalopathy in a boxer Journal Article

In: Acta neuropathologica communications, vol. 2, pp. 24, 2014.

2016

2015

2014

Reference Search

Most Referenced Keywords

2016

2015

2014

About Us

Information