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Marked increase of beta-amyloid(1-42) and amyloid precursor protein in ventricular cerebrospinal fluid after severe traumatic brain injury.

Artikel i vetenskaplig tidskrift
Författare Annika Olsson
Ludvig Z Csajbok
Martin Öst
Kina Höglund
Karin Nylén
Lars Rosengren
Bengt Nellgård
Kaj Blennow
Publicerad i Journal of neurology
Volym 251
Nummer/häfte 7
Sidor 870-6
ISSN 0340-5354
Publiceringsår 2004
Publicerad vid Institutionen för klinisk neurovetenskap
Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Institutionen för de kirurgiska disciplinerna, Avdelningen för anestesiologi och intensivvård
Sidor 870-6
Språk en
Länkar dx.doi.org/10.1007/s00415-004-0451-...
Ämnesord Adult, Alzheimer Disease, etiology, metabolism, physiopathology, Amyloid beta-Protein, blood, cerebrospinal fluid, Amyloid beta-Protein Precursor, cerebrospinal fluid, Biological Markers, blood, cerebrospinal fluid, Brain Injuries, complications, Causality, Cerebral Ventricles, metabolism, Diffuse Axonal Injury, cerebrospinal fluid, etiology, physiopathology, Disease Progression, Female, Humans, Male, Middle Aged, Peptide Fragments, blood, cerebrospinal fluid, Senile Plaques, metabolism, Up-Regulation, physiology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Severe traumatic brain injury (TBI) may result in widespread damage to axons, termed diffuse axonal injury. Alzheimer's disease (AD) is characterised by synaptic and axonal degeneration together with senile plaques (SP). SP are mainly composed of aggregated beta-amyloid (Abeta), which are peptides derived from the amyloid precursor protein (APP). Apart from TBI in itself being considered a risk factor for AD, severe head injury seems to initiate a cascade of molecular events that are also associated with AD. We have therefore analysed the 42 amino acid forms of Abeta (Abeta1-42) and two soluble forms of APP (alpha-sAPP and ss-sAPP) in ventricular cerebrospinal fluid (VCSF) and Abeta(1-42) in plasma from 28 patients in a serial samples 0-11 days after TBI. The levels of alpha-sAPP, ss-sAPP and Abeta(1-42) were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-Abeta(1-42) up to 1173 % from day 0-1 to day 5-6 and in VCSF-beta-sAPP up to 2033 % increase from day 0-1 to day 7-11. There was also a slight but significant increase of VCSF-beta-sAPP from day 0-1 to day 5-6 and day 7-11. By contrast, the plasma- Abeta(1-42) level is unchanged after injury. The marked increase in VCSFAbeta(1-42) implies that increased Abeta expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-Abeta(1-42) in contrast to the marked increase in VCSF-Abeta(1-42) after severe TBI, supports the suggestion that plasma Abeta(1-42) does not reflect Abeta metabolism in the central nervous system (CNS).

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