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},
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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}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
Links | BibTeX | Tags: Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
keywords = {Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)},
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}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
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}
}
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}
}
Baugh, C M; Robbins, C A; Stern, R A; McKee, A C
Current understanding of chronic traumatic encephalopathy Journal Article
In: Current Treatment Options in Neurology, vol. 16, no. 9, 2014.
Links | BibTeX | Tags: Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)
@article{Baugh2014,
title = {Current understanding of chronic traumatic encephalopathy},
author = {Baugh, C M and Robbins, C A and Stern, R A and McKee, A C},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84905669544\&partnerID=40\&md5=b7b1e2fe8132cad56800bf4102896b64},
doi = {10.1007/s11940-014-0306-5},
year = {2014},
date = {2014-01-01},
journal = {Current Treatment Options in Neurology},
volume = {16},
number = {9},
keywords = {Article, attention disturbance, axonal injury, biological marker, Biomarker, Brain trauma, Chronic traumatic encephalopathy, Chronic traumatic encephalopathy (CTE), Chronic Traumatic Encephalopathy APOE, clinical feature, concentration loss, Concussion, degenerative disease, football, genetic risk, headache, human, in vivo study, injury severity, lifestyle, neuropathology, risk factor, Tau, traumatic brain injury, Traumatic brain injury (TBI)},
pubstate = {published},
tppubtype = {article}
}