Journal of Neurology

, Volume 251, Issue 7, pp 870–876

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

Authors

    • Institute of Clinical Neuroscience SectionSahlgrenska University Hospital/Mölndal
  • Ludvig Csajbok
    • Department of Anaesthesia and Intensive Care MedicineSahlgrenska University Hospital
  • Martin Öst
    • Department of Anaesthesia and Intensive Care MedicineSahlgrenska University Hospital
  • Kina Höglund
    • Institute of Clinical Neuroscience SectionSahlgrenska University Hospital/Mölndal
  • Karin Nylén
    • Institute of Clinical NeuroscienceSahlgrenska University Hospital
  • Lars Rosengren
    • Institute of Clinical NeuroscienceSahlgrenska University Hospital
  • Bengt Nellgård
    • Department of Anaesthesia and Intensive Care MedicineSahlgrenska University Hospital
  • Kaj Blennow
    • Institute of Clinical Neuroscience SectionSahlgrenska University Hospital/Mölndal
ORIGINAL COMMUNICATION

DOI: 10.1007/s00415-004-0451-y

Cite this article as:
Olsson, A., Csajbok, L., Öst, M. et al. J Neurol (2004) 251: 870. doi:10.1007/s00415-004-0451-y

Abstract.

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 β-amyloid (Aβ), 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 Aβ (Aβ(1–42)) and two soluble forms of APP (α-sAPP and ßsAPP) in ventricular cerebrospinal fluid (VCSF) and Aβ(1–42) in plasma from 28 patients in a serial samples 0–11 days after TBI. The levels of α-sAPP, ß-sAPP and Aβ(1–42) were determined using ELISA assays. After TBI, there was a significant stepwise increase in VCSF-Aβ(1–42) up to 1173 % from day 0–1 to day 5–6 and in VCSF-β-sAPP up to 2033 % increase from day 0–1 to day 7–11. There was also a slight but significant increase of VCSF-β-sAPP from day 0–1 to day 5–6 and day 7–11. By contrast, the plasma- Aβ(1–42) level is unchanged after injury. The marked increase in VCSFAβ( 1–42) implies that increased Aβ expression may occur as a secondary phenomenon after TBI with axonal damage. The unchanged level of plasma-Aβ(1–42) in contrast to the marked increase in VCSF-Aβ(1–42) after severe TBI, supports the suggestion that plasma Aβ(1–42) does not reflect Aβ metabolism in the central nervous system (CNS).

Key words

Alzheimer’s diseaseamyloid precursor proteinβ-amyloidcerebrospinal fluidtraumatic brain injury

Abbreviations

β-amyloid

AD

Alzheimer’s disease

APLP

amyloid precursor-like proteins

APP

amyloid precursor protein

BBB

blood brain barrier

CT

computed tomography

CNS

central nervous system

GAD

gracile axonal dystrophy

GCS

Glasgow Coma Scale

ICP

intracranial pressure

MRI

magnetic resonance imaging

VCSF

ventricular cerebrospinal fluid

sAPP

soluble amyloid precursor protein

TBI

traumatic brain injury

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© Steinkopff Verlag 2004