Olivera, A; Lejbman, N; Jeromin, A; French, L M; Kim, H S; Cashion, A; Mysliwiec, V; Diaz-Arrastia, R; Gill, J
Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment Journal Article
In: JAMA Neurology, vol. 72, no. 10, pp. 1109–1116, 2015.
Abstract | BibTeX | Tags: *Brain Concussion/me [Metabolism], *Brain Injuries/me [Metabolism], *Depression/me [Metabolism], *Military Personnel, *Stress Disorders, *tau Proteins/bl [Blood], 0 (tau Proteins), 2003-2011, adult, Afghan Campaign 2001-, Brain Concussion/co [Complications], Brain Concussion/di [Diagnosis], Brain Injuries/co [Complications], Brain Injuries/di [Diagnosis], Depression/co [Complications], Depression/di [Diagnosis], Female, Humans, Iraq War, Male, Post-Traumatic/di [Diagnosis], Post-Traumatic/me [Metabolism], Retrospective Studies, self report, Stress Disorders, Young Adult
@article{Olivera2015,
title = {Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment},
author = {Olivera, A and Lejbman, N and Jeromin, A and French, L M and Kim, H S and Cashion, A and Mysliwiec, V and Diaz-Arrastia, R and Gill, J},
year = {2015},
date = {2015-01-01},
journal = {JAMA Neurology},
volume = {72},
number = {10},
pages = {1109--1116},
abstract = {IMPORTANCE: Approximately one-third of military personnel who deploy for combat operations sustain 1 or more traumatic brain injuries (TBIs), which increases the risk for chronic symptoms of postconcussive disorder, posttraumatic stress disorder, and depression and for the development of chronic traumatic encephalopathy. Elevated concentrations of tau are observed in blood shortly following a TBI, but, to our knowledge, the role of tau elevations in blood in the onset and maintenance of chronic symptoms after TBI has not been investigated. OBJECTIVES: To assess peripheral tau levels in military personnel exposed to TBI and to examine the relationship between chronic neurological symptoms and tau elevations. DESIGN, SETTING, AND PARTICIPANTS: Observational assessment from September 2012 to August 2014 of US military personnel at the Madigan Army Medical Center who had been deployed within the previous 18 months. Plasma total tau concentrations were measured using a novel ultrasensitive single-molecule enzyme-linked immunosorbent assay. Classification of participants with and without self-reported TBI was made using the Warrior Administered Retrospective Casualty Assessment Tool. Self-reported symptoms of postconcussive disorder, posttraumatic stress disorder, and depression were determined by the Neurobehavioral Symptom Inventory, the Posttraumatic Stress Disorder Checklist Military Version, and the Quick Inventory of Depressive Symptomatology, respectively. Group differences in tau concentrations were determined through analysis of variance models, and area under the receiver operating characteristic curve determined the sensitivity and specificity of tau concentrations in predicting TBI and chronic symptoms. Seventy participants with self-reported TBI on the Warrior Administered Retrospective Casualty Assessment Tool and 28 control participants with no TBI exposure were included. MAIN OUTCOMES AND MEASURES: Concentration of total tau in peripheral blood. RESULTS: Concentrations of plasma tau were significantly elevated in the 70 participants with self-reported TBI compared with the 28 controls (mean [SD], 1.13 [0.78] vs 0.63 [0.48] pg/mL, respectively; F1},
keywords = {*Brain Concussion/me [Metabolism], *Brain Injuries/me [Metabolism], *Depression/me [Metabolism], *Military Personnel, *Stress Disorders, *tau Proteins/bl [Blood], 0 (tau Proteins), 2003-2011, adult, Afghan Campaign 2001-, Brain Concussion/co [Complications], Brain Concussion/di [Diagnosis], Brain Injuries/co [Complications], Brain Injuries/di [Diagnosis], Depression/co [Complications], Depression/di [Diagnosis], Female, Humans, Iraq War, Male, Post-Traumatic/di [Diagnosis], Post-Traumatic/me [Metabolism], Retrospective Studies, self report, Stress Disorders, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Hamberger, A; Huang, Y L; Zhu, H; Bao, F; Ding, M; Blennow, K; Olsson, A; Hansson, H A; Viano, D; Haglid, K G
Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head Journal Article
In: Journal of Neurotrauma, vol. 20, no. 2, pp. 169–178, 2003.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injuries/me [Metabolism], *Brain/me [Metabolism], *Neurofilament Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (neurofilament protein L), 0 (Neurofilament Proteins), 108688-71-7 (neurofilament protein H), Acceleration, Animals, Brain Injuries/et [Etiology], immunohistochemistry, Phosphorylation, Rabbits, Rotation, Tissue Distribution
@article{Hamberger2003,
title = {Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head},
author = {Hamberger, A and Huang, Y L and Zhu, H and Bao, F and Ding, M and Blennow, K and Olsson, A and Hansson, H A and Viano, D and Haglid, K G},
year = {2003},
date = {2003-01-01},
journal = {Journal of Neurotrauma},
volume = {20},
number = {2},
pages = {169--178},
abstract = {Rotational acceleration of the head, as occurs in falls, car crashes, and sport injuries, may result in diffuse brain damage, with acute and chronic neurological and psychiatric symptoms. The present study addresses the effects of rotational trauma on the neuronal cytoskeleton, which stabilizes perikaryal, dendritic and axonal shape and function. The study focuses upon the distribution of (1) the phosphorylated form of the heavy neurofilament subunit, (2) the light neurofilament subunit, and (3) beta-amyloid, a marker for brain injury. While normally restricted to axons, the phosphorylated heavy neurofilament subunits were drastically decreased in the axons after rotational trauma. Instead, they accumulated in the neuronal perikarya, normally devoid of the phosphorylated subunit. This alteration was seen, not only in the cerebral cortex, but also in the hippocampus, the cervical spinal cord, the cerebellum, the cranial nerves and the pyramidal tract. The distribution of the light subunit of neurofilaments was also altered post trauma. Only a weak beta-amyloid immunoreactivity was detected in the brains of control animals. Promptly after the trauma, a large number of beta-amyloid positive neurons appeared. Intensely co-localized immunoreactivity for the light subunit of neurofilaments and of beta-amyloid was seen 3 days after the rotational trauma axons of in the subcortical white matter and in the granule cell layer of the dentate gyrus as well as in neurons of the hypoglossal nucleus. The reported alterations in the central nervous system neurons are similar to those in the human brain after closed head injury and in chronic degenerative diseases. Regions of importance for social behavior, memory and body movement were affected.},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injuries/me [Metabolism], *Brain/me [Metabolism], *Neurofilament Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (neurofilament protein L), 0 (Neurofilament Proteins), 108688-71-7 (neurofilament protein H), Acceleration, Animals, Brain Injuries/et [Etiology], immunohistochemistry, Phosphorylation, Rabbits, Rotation, Tissue Distribution},
pubstate = {published},
tppubtype = {article}
}
Olivera, A; Lejbman, N; Jeromin, A; French, L M; Kim, H S; Cashion, A; Mysliwiec, V; Diaz-Arrastia, R; Gill, J
Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment Journal Article
In: JAMA Neurology, vol. 72, no. 10, pp. 1109–1116, 2015.
@article{Olivera2015,
title = {Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment},
author = {Olivera, A and Lejbman, N and Jeromin, A and French, L M and Kim, H S and Cashion, A and Mysliwiec, V and Diaz-Arrastia, R and Gill, J},
year = {2015},
date = {2015-01-01},
journal = {JAMA Neurology},
volume = {72},
number = {10},
pages = {1109--1116},
abstract = {IMPORTANCE: Approximately one-third of military personnel who deploy for combat operations sustain 1 or more traumatic brain injuries (TBIs), which increases the risk for chronic symptoms of postconcussive disorder, posttraumatic stress disorder, and depression and for the development of chronic traumatic encephalopathy. Elevated concentrations of tau are observed in blood shortly following a TBI, but, to our knowledge, the role of tau elevations in blood in the onset and maintenance of chronic symptoms after TBI has not been investigated. OBJECTIVES: To assess peripheral tau levels in military personnel exposed to TBI and to examine the relationship between chronic neurological symptoms and tau elevations. DESIGN, SETTING, AND PARTICIPANTS: Observational assessment from September 2012 to August 2014 of US military personnel at the Madigan Army Medical Center who had been deployed within the previous 18 months. Plasma total tau concentrations were measured using a novel ultrasensitive single-molecule enzyme-linked immunosorbent assay. Classification of participants with and without self-reported TBI was made using the Warrior Administered Retrospective Casualty Assessment Tool. Self-reported symptoms of postconcussive disorder, posttraumatic stress disorder, and depression were determined by the Neurobehavioral Symptom Inventory, the Posttraumatic Stress Disorder Checklist Military Version, and the Quick Inventory of Depressive Symptomatology, respectively. Group differences in tau concentrations were determined through analysis of variance models, and area under the receiver operating characteristic curve determined the sensitivity and specificity of tau concentrations in predicting TBI and chronic symptoms. Seventy participants with self-reported TBI on the Warrior Administered Retrospective Casualty Assessment Tool and 28 control participants with no TBI exposure were included. MAIN OUTCOMES AND MEASURES: Concentration of total tau in peripheral blood. RESULTS: Concentrations of plasma tau were significantly elevated in the 70 participants with self-reported TBI compared with the 28 controls (mean [SD], 1.13 [0.78] vs 0.63 [0.48] pg/mL, respectively; F1},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Hamberger, A; Huang, Y L; Zhu, H; Bao, F; Ding, M; Blennow, K; Olsson, A; Hansson, H A; Viano, D; Haglid, K G
Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head Journal Article
In: Journal of Neurotrauma, vol. 20, no. 2, pp. 169–178, 2003.
@article{Hamberger2003,
title = {Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head},
author = {Hamberger, A and Huang, Y L and Zhu, H and Bao, F and Ding, M and Blennow, K and Olsson, A and Hansson, H A and Viano, D and Haglid, K G},
year = {2003},
date = {2003-01-01},
journal = {Journal of Neurotrauma},
volume = {20},
number = {2},
pages = {169--178},
abstract = {Rotational acceleration of the head, as occurs in falls, car crashes, and sport injuries, may result in diffuse brain damage, with acute and chronic neurological and psychiatric symptoms. The present study addresses the effects of rotational trauma on the neuronal cytoskeleton, which stabilizes perikaryal, dendritic and axonal shape and function. The study focuses upon the distribution of (1) the phosphorylated form of the heavy neurofilament subunit, (2) the light neurofilament subunit, and (3) beta-amyloid, a marker for brain injury. While normally restricted to axons, the phosphorylated heavy neurofilament subunits were drastically decreased in the axons after rotational trauma. Instead, they accumulated in the neuronal perikarya, normally devoid of the phosphorylated subunit. This alteration was seen, not only in the cerebral cortex, but also in the hippocampus, the cervical spinal cord, the cerebellum, the cranial nerves and the pyramidal tract. The distribution of the light subunit of neurofilaments was also altered post trauma. Only a weak beta-amyloid immunoreactivity was detected in the brains of control animals. Promptly after the trauma, a large number of beta-amyloid positive neurons appeared. Intensely co-localized immunoreactivity for the light subunit of neurofilaments and of beta-amyloid was seen 3 days after the rotational trauma axons of in the subcortical white matter and in the granule cell layer of the dentate gyrus as well as in neurons of the hypoglossal nucleus. The reported alterations in the central nervous system neurons are similar to those in the human brain after closed head injury and in chronic degenerative diseases. Regions of importance for social behavior, memory and body movement were affected.},
keywords = {},
pubstate = {published},
tppubtype = {article}
}
Olivera, A; Lejbman, N; Jeromin, A; French, L M; Kim, H S; Cashion, A; Mysliwiec, V; Diaz-Arrastia, R; Gill, J
Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment Journal Article
In: JAMA Neurology, vol. 72, no. 10, pp. 1109–1116, 2015.
Abstract | BibTeX | Tags: *Brain Concussion/me [Metabolism], *Brain Injuries/me [Metabolism], *Depression/me [Metabolism], *Military Personnel, *Stress Disorders, *tau Proteins/bl [Blood], 0 (tau Proteins), 2003-2011, adult, Afghan Campaign 2001-, Brain Concussion/co [Complications], Brain Concussion/di [Diagnosis], Brain Injuries/co [Complications], Brain Injuries/di [Diagnosis], Depression/co [Complications], Depression/di [Diagnosis], Female, Humans, Iraq War, Male, Post-Traumatic/di [Diagnosis], Post-Traumatic/me [Metabolism], Retrospective Studies, self report, Stress Disorders, Young Adult
@article{Olivera2015,
title = {Peripheral Total Tau in Military Personnel Who Sustain Traumatic Brain Injuries During Deployment},
author = {Olivera, A and Lejbman, N and Jeromin, A and French, L M and Kim, H S and Cashion, A and Mysliwiec, V and Diaz-Arrastia, R and Gill, J},
year = {2015},
date = {2015-01-01},
journal = {JAMA Neurology},
volume = {72},
number = {10},
pages = {1109--1116},
abstract = {IMPORTANCE: Approximately one-third of military personnel who deploy for combat operations sustain 1 or more traumatic brain injuries (TBIs), which increases the risk for chronic symptoms of postconcussive disorder, posttraumatic stress disorder, and depression and for the development of chronic traumatic encephalopathy. Elevated concentrations of tau are observed in blood shortly following a TBI, but, to our knowledge, the role of tau elevations in blood in the onset and maintenance of chronic symptoms after TBI has not been investigated. OBJECTIVES: To assess peripheral tau levels in military personnel exposed to TBI and to examine the relationship between chronic neurological symptoms and tau elevations. DESIGN, SETTING, AND PARTICIPANTS: Observational assessment from September 2012 to August 2014 of US military personnel at the Madigan Army Medical Center who had been deployed within the previous 18 months. Plasma total tau concentrations were measured using a novel ultrasensitive single-molecule enzyme-linked immunosorbent assay. Classification of participants with and without self-reported TBI was made using the Warrior Administered Retrospective Casualty Assessment Tool. Self-reported symptoms of postconcussive disorder, posttraumatic stress disorder, and depression were determined by the Neurobehavioral Symptom Inventory, the Posttraumatic Stress Disorder Checklist Military Version, and the Quick Inventory of Depressive Symptomatology, respectively. Group differences in tau concentrations were determined through analysis of variance models, and area under the receiver operating characteristic curve determined the sensitivity and specificity of tau concentrations in predicting TBI and chronic symptoms. Seventy participants with self-reported TBI on the Warrior Administered Retrospective Casualty Assessment Tool and 28 control participants with no TBI exposure were included. MAIN OUTCOMES AND MEASURES: Concentration of total tau in peripheral blood. RESULTS: Concentrations of plasma tau were significantly elevated in the 70 participants with self-reported TBI compared with the 28 controls (mean [SD], 1.13 [0.78] vs 0.63 [0.48] pg/mL, respectively; F1},
keywords = {*Brain Concussion/me [Metabolism], *Brain Injuries/me [Metabolism], *Depression/me [Metabolism], *Military Personnel, *Stress Disorders, *tau Proteins/bl [Blood], 0 (tau Proteins), 2003-2011, adult, Afghan Campaign 2001-, Brain Concussion/co [Complications], Brain Concussion/di [Diagnosis], Brain Injuries/co [Complications], Brain Injuries/di [Diagnosis], Depression/co [Complications], Depression/di [Diagnosis], Female, Humans, Iraq War, Male, Post-Traumatic/di [Diagnosis], Post-Traumatic/me [Metabolism], Retrospective Studies, self report, Stress Disorders, Young Adult},
pubstate = {published},
tppubtype = {article}
}
Hamberger, A; Huang, Y L; Zhu, H; Bao, F; Ding, M; Blennow, K; Olsson, A; Hansson, H A; Viano, D; Haglid, K G
Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head Journal Article
In: Journal of Neurotrauma, vol. 20, no. 2, pp. 169–178, 2003.
Abstract | BibTeX | Tags: *Amyloid beta-Peptides/me [Metabolism], *Brain Injuries/me [Metabolism], *Brain/me [Metabolism], *Neurofilament Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (neurofilament protein L), 0 (Neurofilament Proteins), 108688-71-7 (neurofilament protein H), Acceleration, Animals, Brain Injuries/et [Etiology], immunohistochemistry, Phosphorylation, Rabbits, Rotation, Tissue Distribution
@article{Hamberger2003,
title = {Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head},
author = {Hamberger, A and Huang, Y L and Zhu, H and Bao, F and Ding, M and Blennow, K and Olsson, A and Hansson, H A and Viano, D and Haglid, K G},
year = {2003},
date = {2003-01-01},
journal = {Journal of Neurotrauma},
volume = {20},
number = {2},
pages = {169--178},
abstract = {Rotational acceleration of the head, as occurs in falls, car crashes, and sport injuries, may result in diffuse brain damage, with acute and chronic neurological and psychiatric symptoms. The present study addresses the effects of rotational trauma on the neuronal cytoskeleton, which stabilizes perikaryal, dendritic and axonal shape and function. The study focuses upon the distribution of (1) the phosphorylated form of the heavy neurofilament subunit, (2) the light neurofilament subunit, and (3) beta-amyloid, a marker for brain injury. While normally restricted to axons, the phosphorylated heavy neurofilament subunits were drastically decreased in the axons after rotational trauma. Instead, they accumulated in the neuronal perikarya, normally devoid of the phosphorylated subunit. This alteration was seen, not only in the cerebral cortex, but also in the hippocampus, the cervical spinal cord, the cerebellum, the cranial nerves and the pyramidal tract. The distribution of the light subunit of neurofilaments was also altered post trauma. Only a weak beta-amyloid immunoreactivity was detected in the brains of control animals. Promptly after the trauma, a large number of beta-amyloid positive neurons appeared. Intensely co-localized immunoreactivity for the light subunit of neurofilaments and of beta-amyloid was seen 3 days after the rotational trauma axons of in the subcortical white matter and in the granule cell layer of the dentate gyrus as well as in neurons of the hypoglossal nucleus. The reported alterations in the central nervous system neurons are similar to those in the human brain after closed head injury and in chronic degenerative diseases. Regions of importance for social behavior, memory and body movement were affected.},
keywords = {*Amyloid beta-Peptides/me [Metabolism], *Brain Injuries/me [Metabolism], *Brain/me [Metabolism], *Neurofilament Proteins/me [Metabolism], 0 (Amyloid beta-Peptides), 0 (neurofilament protein L), 0 (Neurofilament Proteins), 108688-71-7 (neurofilament protein H), Acceleration, Animals, Brain Injuries/et [Etiology], immunohistochemistry, Phosphorylation, Rabbits, Rotation, Tissue Distribution},
pubstate = {published},
tppubtype = {article}
}