Influence of the blood-CSF-barrier function on S100B in neurodegenerative diseases
Article first published online: 19 MAR 2013
© 2013 John Wiley & Sons A/S
Acta Neurologica Scandinavica
Volume 128, Issue 4, pages 249–256, October 2013
How to Cite
Influence of the blood-CSF-barrier function on S100B in neurodegenerative diseases. Acta Neurol Scand 2013: 128: 249–256. © 2013 John Wiley & Sons A/S., , , , , .
- Issue published online: 10 SEP 2013
- Article first published online: 19 MAR 2013
- Manuscript Accepted: 22 JAN 2013
- Bundesministerium für Bildung und Forschung
- European Union (Anteprion, Sophia, BiomarkAPD, FTLDc, Nadine)
- albumin quotient;
- blood-cerebrospinal fluid barrier;
- cerebrospinal fluid flow;
- Creutzfeldt-Jakob disease;
S100B was proposed to be a CSF and blood biomarker in a number of neurological diseases. The route of S100B to the CSF and the blood in neurodegenerative diseases is unclear. To assess the impact of the physiological or impaired blood-CSF-barrier (BCSFB) function on S100B concentrations in CSF and serum, we analysed S100B in correlation of the albumin quotient.
Materials and methods
S100Bserum and S100BCSF were quantified in samples from patients with a variety of neurological diseases using an immunoluminometric assay (Sangtec LIA-mat). Measures were analysed for a potential relation to the CSF/serum-albumin quotient (Qalb), which indicates the BCSFB functionality.
We reasserted increased S100B concentrations in CSF and serum of CJD patients. Elevated S100Bserum correlated with elevated S100BCSF in all diagnoses but with exceptions. Neither S100BCSF nor S100Bserum did correlate with Qalb, even when the BCSFB function was progressively impaired as demonstrated by increased Qalb.
The lack of correlation between Qalb and S100BCSF is typically seen for proteins which are brain derived. Therefore, we propose that S100B enters the blood with the bulk flow via Pacchioni's granules and along the spinal nerve sheaths.