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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
Abstract | Links | BibTeX | Tags: Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
keywords = {Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling},
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}
}
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}
}
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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
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}
}
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 = {},
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}
}
Edlow, B L; Hinson, H E
Blowing the whistle on sports concussions Journal Article
In: Neurology, vol. 85, no. 17, pp. 1442–1443, 2015.
Abstract | Links | BibTeX | Tags: Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling
@article{Edlow2015,
title = {Blowing the whistle on sports concussions},
author = {Edlow, B L and Hinson, H E},
doi = {10.1212/WNL.0000000000001902},
year = {2015},
date = {2015-01-01},
journal = {Neurology},
volume = {85},
number = {17},
pages = {1442--1443},
abstract = {On March 13, 2015, Chris Borland, a star rookie linebacker on the San Francisco 49ers, announced his early retirement from professional football, citing concerns about chronic traumatic encephalopathy (CTE). Borland, who had a history of 2 diagnosed concussions, walked away from a multi-million-dollar contract and potential sports superstardom, explaining that "from what I've researched and what I've experienced, I don't think it's worth the risk." 1 Perhaps just as surprising as Borland's announcement was the support he received from teammates and other athletes-support that reflects a growing recognition in the athletic community that repetitive head trauma may be associated with CTE and other forms of dementia. 2 Indeed, in a recent legal settlement, the National Football League estimated that approximately 30% of its former players will develop dementia. At the high school and college levels, state legislatures and universities have enacted limits to the number of full-contact practices, citing similar concerns about concussions. These developments have prompted a societal conversation about the risks of contact sports. © 2015 American Academy of Neurology.},
keywords = {Alzheimer disease, Chronic traumatic encephalopathy, Concussion, contact sport, Diffusion Tensor Imaging, football, functional magnetic resonance imaging, histopathology, Hockey, human, memory disorder, mood disorder, pathogenesis, Pathophysiology, priority journal, Review, rugby, Soccer, sport injury, sports concussion, traumatic brain injury, wrestling},
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}
}
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}
}