title: Redistribution of neurofilaments and accumulation of beta-amyloid protein after brain injury by rotational acceleration of the head.
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.
authors.affiliation: Institute of Anatomy and Cell Biology, University of Göteborg, Göteborg, Sweden. anders.hamberger@anatcell.gu.se
authors.forename: Anders
authors.initials: A
authors.lastname: Hamberger
authors.forename: Ying-Lai
authors.initials: YL
authors.lastname: Huang
authors.forename: Hong
authors.initials: H
authors.lastname: Zhu
authors.forename: Feng
authors.initials: F
authors.lastname: Bao
authors.forename: Mei
authors.initials: M
authors.lastname: Ding
authors.forename: Kaj
authors.initials: K
authors.lastname: Blennow
authors.forename: Annika
authors.initials: A
authors.lastname: Olsson
authors.forename: Hans-Arne
authors.initials: HA
authors.lastname: Hansson
authors.forename: David
authors.initials: D
authors.lastname: Viano
authors.forename: Kenneth G
authors.initials: KG
authors.lastname: Haglid
mesh_terms: D000054:Acceleration; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000209:etiology / Q000378:metabolism*; D007150:Immunohistochemistry; D016900:Neurofilament Proteins / Q000378:metabolism*; D010766:Phosphorylation; D011817:Rabbits; D012399:Rotation; D014018:Tissue Distribution
chemical_list: D016229:Amyloid beta-Peptides; D016900:Neurofilament Proteins; C044882:neurofilament protein L; C051774:neurofilament protein H