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}

}

Oliver, J M; Jones, M T; Kirk, K M; Gable, D A; Repshas, J T; Johnson, T A; Andréasson, U; Norgren, N; Blennow, K; Zetterberg, H

Serum Neurofilament Light in American Football Athletes over the Course of a Season Journal Article

In: Journal of Neurotrauma, vol. 33, no. 19, pp. 1784–1789, 2016.

Abstract | Links | BibTeX | Tags: adult brain injury, axonal injury, Biomarkers, Head trauma, traumatic brain injury

@article{Oliver2016,

title = {Serum Neurofilament Light in American Football Athletes over the Course of a Season},

author = {Oliver, J M and Jones, M T and Kirk, K M and Gable, D A and Repshas, J T and Johnson, T A and Andr\'{e}asson, U and Norgren, N and Blennow, K and Zetterberg, H},

doi = {10.1089/neu.2015.4295},

year  = {2016},

date = {2016-01-01},

journal = {Journal of Neurotrauma},

volume = {33},

number = {19},

pages = {1784--1789},

abstract = {Despite being underreported, American football boasts the highest incidence of concussion among all team sports, likely due to exposure to head impacts that vary in number and magnitude over the season. This study compared a biological marker of head trauma in American football athletes with non-contact sport athletes and examined changes over the course of a season. Baseline serum neurofilament light polypeptide (NFL) was measured after 9 weeks of no contact and compared with a non-contact sport. Serum NFL was then measured over the course of the entire season at eight time-points coincident with expected changes in likelihood of increased head impacts. Data were compared between starters (n = 11) and non-starters (n = 9). Compared with non-starters (mean ± standard deviation) (7.30 ± 3.57 pg•mL-1) and controls (6.75 ± 1.68 pg•mL-1), serum NFL in starters (8.45 ± 5.90 pg•mL-1) was higher at baseline (mean difference; ±90% confidence interval) (1.69; ± 1.96 pg•mL-1 and 1.15; ± 1.4 pg•mL-1, respectively). Over the course of the season, an increase (effect size [ES] = 1.8; p \< 0.001) was observed post-camp relative to baseline (1.52 ± 1.18 pg•mL-1), which remained elevated until conference play, when a second increase was observed (ES = 2.6; p = 0.008) over baseline (4.82 ± 2.64 pg•mL-1). A lack of change in non-starters resulted in substantial differences between starters and non-starters over the course of the season. These data suggest that a season of collegiate American football is associated with elevations in serum NFL, which is indicative of axonal injury, as a result of head impacts. Copyright © 2016, Mary Ann Liebert, Inc.},

keywords = {adult brain injury, axonal injury, Biomarkers, Head trauma, traumatic brain injury},

pubstate = {published},

tppubtype = {article}

}

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.)

2014

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)

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

Oliver, J M; Jones, M T; Kirk, K M; Gable, D A; Repshas, J T; Johnson, T A; Andréasson, U; Norgren, N; Blennow, K; Zetterberg, H

Serum Neurofilament Light in American Football Athletes over the Course of a Season Journal Article

In: Journal of Neurotrauma, vol. 33, no. 19, pp. 1784–1789, 2016.

Abstract | Links | BibTeX

@article{Oliver2016,

title = {Serum Neurofilament Light in American Football Athletes over the Course of a Season},

author = {Oliver, J M and Jones, M T and Kirk, K M and Gable, D A and Repshas, J T and Johnson, T A and Andr\'{e}asson, U and Norgren, N and Blennow, K and Zetterberg, H},

doi = {10.1089/neu.2015.4295},

year  = {2016},

date = {2016-01-01},

journal = {Journal of Neurotrauma},

volume = {33},

number = {19},

pages = {1784--1789},

abstract = {Despite being underreported, American football boasts the highest incidence of concussion among all team sports, likely due to exposure to head impacts that vary in number and magnitude over the season. This study compared a biological marker of head trauma in American football athletes with non-contact sport athletes and examined changes over the course of a season. Baseline serum neurofilament light polypeptide (NFL) was measured after 9 weeks of no contact and compared with a non-contact sport. Serum NFL was then measured over the course of the entire season at eight time-points coincident with expected changes in likelihood of increased head impacts. Data were compared between starters (n = 11) and non-starters (n = 9). Compared with non-starters (mean ± standard deviation) (7.30 ± 3.57 pg•mL-1) and controls (6.75 ± 1.68 pg•mL-1), serum NFL in starters (8.45 ± 5.90 pg•mL-1) was higher at baseline (mean difference; ±90% confidence interval) (1.69; ± 1.96 pg•mL-1 and 1.15; ± 1.4 pg•mL-1, respectively). Over the course of the season, an increase (effect size [ES] = 1.8; p \< 0.001) was observed post-camp relative to baseline (1.52 ± 1.18 pg•mL-1), which remained elevated until conference play, when a second increase was observed (ES = 2.6; p = 0.008) over baseline (4.82 ± 2.64 pg•mL-1). A lack of change in non-starters resulted in substantial differences between starters and non-starters over the course of the season. These data suggest that a season of collegiate American football is associated with elevations in serum NFL, which is indicative of axonal injury, as a result of head impacts. Copyright © 2016, Mary Ann Liebert, Inc.},

keywords = {},

pubstate = {published},

tppubtype = {article}

}

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}

}

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

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}

}

Oliver, J M; Jones, M T; Kirk, K M; Gable, D A; Repshas, J T; Johnson, T A; Andréasson, U; Norgren, N; Blennow, K; Zetterberg, H

Serum Neurofilament Light in American Football Athletes over the Course of a Season Journal Article

In: Journal of Neurotrauma, vol. 33, no. 19, pp. 1784–1789, 2016.

Abstract | Links | BibTeX | Tags: adult brain injury, axonal injury, Biomarkers, Head trauma, traumatic brain injury

@article{Oliver2016,

title = {Serum Neurofilament Light in American Football Athletes over the Course of a Season},

author = {Oliver, J M and Jones, M T and Kirk, K M and Gable, D A and Repshas, J T and Johnson, T A and Andr\'{e}asson, U and Norgren, N and Blennow, K and Zetterberg, H},

doi = {10.1089/neu.2015.4295},

year  = {2016},

date = {2016-01-01},

journal = {Journal of Neurotrauma},

volume = {33},

number = {19},

pages = {1784--1789},

abstract = {Despite being underreported, American football boasts the highest incidence of concussion among all team sports, likely due to exposure to head impacts that vary in number and magnitude over the season. This study compared a biological marker of head trauma in American football athletes with non-contact sport athletes and examined changes over the course of a season. Baseline serum neurofilament light polypeptide (NFL) was measured after 9 weeks of no contact and compared with a non-contact sport. Serum NFL was then measured over the course of the entire season at eight time-points coincident with expected changes in likelihood of increased head impacts. Data were compared between starters (n = 11) and non-starters (n = 9). Compared with non-starters (mean ± standard deviation) (7.30 ± 3.57 pg•mL-1) and controls (6.75 ± 1.68 pg•mL-1), serum NFL in starters (8.45 ± 5.90 pg•mL-1) was higher at baseline (mean difference; ±90% confidence interval) (1.69; ± 1.96 pg•mL-1 and 1.15; ± 1.4 pg•mL-1, respectively). Over the course of the season, an increase (effect size [ES] = 1.8; p \< 0.001) was observed post-camp relative to baseline (1.52 ± 1.18 pg•mL-1), which remained elevated until conference play, when a second increase was observed (ES = 2.6; p = 0.008) over baseline (4.82 ± 2.64 pg•mL-1). A lack of change in non-starters resulted in substantial differences between starters and non-starters over the course of the season. These data suggest that a season of collegiate American football is associated with elevations in serum NFL, which is indicative of axonal injury, as a result of head impacts. Copyright © 2016, Mary Ann Liebert, Inc.},

keywords = {adult brain injury, axonal injury, Biomarkers, Head trauma, traumatic brain injury},

pubstate = {published},

tppubtype = {article}

}

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}

}

2014

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.

2016

2015

2014

Reference Search

Most Referenced Keywords

2016

2015

2014

About Us

Information