Neselius, S; Brisby, H; Granholm, F; Zetterberg, H; Blennow, K
Monitoring concussion in a knocked-out boxer by CSF biomarker analysis Journal Article
In: Knee Surgery, Sports Traumatology, Arthroscopy, vol. 23, no. 9, pp. 2536–2539, 2015.
Abstract | BibTeX | Tags: *Boxing/in [Injuries], *Brain Concussion/di [Diagnosis], *Neurofilament Proteins/cf [Cerebrospinal Fluid], 0 (Biomarkers), 0 (neurofilament protein L), 0 (Neurofilament Proteins), Biomarkers/cf [Cerebrospinal Fluid], Brain Concussion/cf [Cerebrospinal Fluid], Brain Concussion/et [Etiology], Humans, Male, Young Adult
@article{Neselius2015,
title = {Monitoring concussion in a knocked-out boxer by CSF biomarker analysis},
author = {Neselius, S and Brisby, H and Granholm, F and Zetterberg, H and Blennow, K},
year = {2015},
date = {2015-01-01},
journal = {Knee Surgery, Sports Traumatology, Arthroscopy},
volume = {23},
number = {9},
pages = {2536--2539},
abstract = {Concussion is common in many sports, and the incidence is increasing. The medical consequences after a sport-related concussion have received increased attention in recent years since it is known that concussions cause axonal and glial damage, which disturbs the cerebral physiology and makes the brain more vulnerable for additional concussions. This study reports on a knocked-out amateur boxer in whom cerebrospinal fluid (CSF) neurofilament light (NFL) protein, reflecting axonal damage, was used to identify and monitor brain damage. CSF NFL was markedly increased during 36 weeks, suggesting that neuronal injury persists longer than expected after a concussion. CSF biomarker analysis may be valuable in the medical counselling of concussed athletes and in return-to-play considerations.},
keywords = {*Boxing/in [Injuries], *Brain Concussion/di [Diagnosis], *Neurofilament Proteins/cf [Cerebrospinal Fluid], 0 (Biomarkers), 0 (neurofilament protein L), 0 (Neurofilament Proteins), Biomarkers/cf [Cerebrospinal Fluid], Brain Concussion/cf [Cerebrospinal Fluid], Brain Concussion/et [Etiology], Humans, Male, 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}
}
Neselius, S; Brisby, H; Granholm, F; Zetterberg, H; Blennow, K
Monitoring concussion in a knocked-out boxer by CSF biomarker analysis Journal Article
In: Knee Surgery, Sports Traumatology, Arthroscopy, vol. 23, no. 9, pp. 2536–2539, 2015.
@article{Neselius2015,
title = {Monitoring concussion in a knocked-out boxer by CSF biomarker analysis},
author = {Neselius, S and Brisby, H and Granholm, F and Zetterberg, H and Blennow, K},
year = {2015},
date = {2015-01-01},
journal = {Knee Surgery, Sports Traumatology, Arthroscopy},
volume = {23},
number = {9},
pages = {2536--2539},
abstract = {Concussion is common in many sports, and the incidence is increasing. The medical consequences after a sport-related concussion have received increased attention in recent years since it is known that concussions cause axonal and glial damage, which disturbs the cerebral physiology and makes the brain more vulnerable for additional concussions. This study reports on a knocked-out amateur boxer in whom cerebrospinal fluid (CSF) neurofilament light (NFL) protein, reflecting axonal damage, was used to identify and monitor brain damage. CSF NFL was markedly increased during 36 weeks, suggesting that neuronal injury persists longer than expected after a concussion. CSF biomarker analysis may be valuable in the medical counselling of concussed athletes and in return-to-play considerations.},
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}
}
Neselius, S; Brisby, H; Granholm, F; Zetterberg, H; Blennow, K
Monitoring concussion in a knocked-out boxer by CSF biomarker analysis Journal Article
In: Knee Surgery, Sports Traumatology, Arthroscopy, vol. 23, no. 9, pp. 2536–2539, 2015.
Abstract | BibTeX | Tags: *Boxing/in [Injuries], *Brain Concussion/di [Diagnosis], *Neurofilament Proteins/cf [Cerebrospinal Fluid], 0 (Biomarkers), 0 (neurofilament protein L), 0 (Neurofilament Proteins), Biomarkers/cf [Cerebrospinal Fluid], Brain Concussion/cf [Cerebrospinal Fluid], Brain Concussion/et [Etiology], Humans, Male, Young Adult
@article{Neselius2015,
title = {Monitoring concussion in a knocked-out boxer by CSF biomarker analysis},
author = {Neselius, S and Brisby, H and Granholm, F and Zetterberg, H and Blennow, K},
year = {2015},
date = {2015-01-01},
journal = {Knee Surgery, Sports Traumatology, Arthroscopy},
volume = {23},
number = {9},
pages = {2536--2539},
abstract = {Concussion is common in many sports, and the incidence is increasing. The medical consequences after a sport-related concussion have received increased attention in recent years since it is known that concussions cause axonal and glial damage, which disturbs the cerebral physiology and makes the brain more vulnerable for additional concussions. This study reports on a knocked-out amateur boxer in whom cerebrospinal fluid (CSF) neurofilament light (NFL) protein, reflecting axonal damage, was used to identify and monitor brain damage. CSF NFL was markedly increased during 36 weeks, suggesting that neuronal injury persists longer than expected after a concussion. CSF biomarker analysis may be valuable in the medical counselling of concussed athletes and in return-to-play considerations.},
keywords = {*Boxing/in [Injuries], *Brain Concussion/di [Diagnosis], *Neurofilament Proteins/cf [Cerebrospinal Fluid], 0 (Biomarkers), 0 (neurofilament protein L), 0 (Neurofilament Proteins), Biomarkers/cf [Cerebrospinal Fluid], Brain Concussion/cf [Cerebrospinal Fluid], Brain Concussion/et [Etiology], Humans, Male, 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}
}