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 \& 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},
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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 = {},
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 | 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 \& 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},
pubstate = {published},
tppubtype = {article}
}