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}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
Abstract | Links | BibTeX | Tags: animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Blennow, K; Brody, D L; Kochanek, P M; Levin, H; McKee, A; Ribbers, G M; Yaffe, K; Zetterberg, H
Traumatic brain injuries Journal Article
In: Nature Reviews Disease Primers, vol. 2, 2016.
Abstract | Links | BibTeX | Tags: amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury
@article{Blennow2016,
title = {Traumatic brain injuries},
author = {Blennow, K and Brody, D L and Kochanek, P M and Levin, H and McKee, A and Ribbers, G M and Yaffe, K and Zetterberg, H},
doi = {10.1038/nrdp.2016.84},
year = {2016},
date = {2016-01-01},
journal = {Nature Reviews Disease Primers},
volume = {2},
abstract = {Traumatic brain injuries (TBIs) are clinically grouped by severity: mild, moderate and severe. Mild TBI (the least severe form) is synonymous with concussion and is typically caused by blunt non-penetrating head trauma. The trauma causes stretching and tearing of axons, which leads to diffuse axonal injury-the best-studied pathogenetic mechanism of this disorder. However, mild TBI is defined on clinical grounds and no well-validated imaging or fluid biomarkers to determine the presence of neuronal damage in patients with mild TBI is available. Most patients with mild TBI will recover quickly, but others report persistent symptoms, called post-concussive syndrome, the underlying pathophysiology of which is largely unknown. Repeated concussive and subconcussive head injuries have been linked to the neurodegenerative condition chronic traumatic encephalopathy (CTE), which has been reported post-mortem in contact sports athletes and soldiers exposed to blasts. Insights from severe injuries and CTE plausibly shed light on the underlying cellular and molecular processes involved in mild TBI. MRI techniques and blood tests for axonal proteins to identify and grade axonal injury, in addition to PET for tau pathology, show promise as tools to explore CTE pathophysiology in longitudinal clinical studies, and might be developed into diagnostic tools for CTE. Given that CTE is attributed to repeated head trauma, prevention might be possible through rule changes by sports organizations and legislators. © 2016 Macmillan Publishers Limited, part of Springer Nature.},
keywords = {amyloid beta protein, Article, axonal injury, biological marker, BIOPHYSICS, blood, brain, BRAIN damage, cerebrospinal fluid, Chronic traumatic encephalopathy, computer assisted tomography, disease severity, endocrine disease, heredity, human, molecular pathology, neuropathology, nonhuman, nuclear magnetic resonance imaging, Pathophysiology, positron emission tomography, postconcussion syndrome, priority journal, protein aggregation, quality of life, screening, tau protein, traumatic brain injury},
pubstate = {published},
tppubtype = {article}
}
Gandy, S; Ikonomovic, M D; Mitsis, E; Elder, G; Ahlers, S T; Barth, J; Stone, J R; Dekosky, S T
Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis Journal Article
In: Molecular Neurodegeneration, vol. 9, no. 1, 2014.
Abstract | Links | BibTeX | Tags: animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory
@article{Gandy2014a,
title = {Chronic traumatic encephalopathy: Clinical-biomarker correlations and current concepts in pathogenesis},
author = {Gandy, S and Ikonomovic, M D and Mitsis, E and Elder, G and Ahlers, S T and Barth, J and Stone, J R and Dekosky, S T},
url = {http://www.scopus.com/inward/record.url?eid=2-s2.0-84907464163\&partnerID=40\&md5=109c916e926417c11bab99fd7b44065c},
doi = {10.1186/1750-1326-9-37},
year = {2014},
date = {2014-01-01},
journal = {Molecular Neurodegeneration},
volume = {9},
number = {1},
abstract = {Background: Chronic traumatic encephalopathy (CTE) is a recently revived term used to describe a neurodegenerative process that occurs as a long term complication of repetitive mild traumatic brain injury (TBI). Corsellis provided one of the classic descriptions of CTE in boxers under the name "dementia pugilistica" (DP). Much recent attention has been drawn to the apparent association of CTE with contact sports (football, soccer, hockey) and with frequent battlefield exposure to blast waves generated by improvised explosive devices (IEDs). Recently, a promising serum biomarker has been identified by measurement of serum levels of the neuronal microtubule associated protein tau. New positron emission tomography (PET) ligands (e.g., [18F] T807) that identify brain tauopathy have been successfully deployed for the in vitro and in vivo detection of presumptive tauopathy in the brains of subjects with clinically probable CTE. Methods. Major academic and lay publications on DP/CTE were reviewed beginning with the 1928 paper describing the initial use of the term CTE by Martland. Results: The major current concepts in the neurological, psychiatric, neuropsychological, neuroimaging, and body fluid biomarker science of DP/CTE have been summarized. Newer achievements, such as serum tau and [18F] T807 tauopathy imaging, are also introduced and their significance has been explained. Conclusion: Recent advances in the science of DP/CTE hold promise for elucidating a long sought accurate determination of the true prevalence of CTE. This information holds potentially important public health implications for estimating the risk of contact sports in inflicting permanent and/or progressive brain damage on children, adolescents, and adults. © 2014Gandy et al.; licensee BioMed Central Ltd.},
keywords = {animal model, army, Article, blast injury, body fluid, Boxing, chronic disease, Chronic traumatic encephalopathy, Chronic Traumatic Encephalopathy biological marker, Dementia, dementia pugilistica, Diffusion Tensor Imaging, executive function, experimental animal, fluorine 18, football, functional magnetic resonance imaging, functional neuroimaging, human, molecular pathology, neuropathology, neuropsychology, nonhuman, nuclear magnetic resonance imaging, Occupational Exposure, positron emission tomography, punch drunk syndrome, systematic review (topic), traumatic brain injury, white matter, working memory},
pubstate = {published},
tppubtype = {article}
}