Influence of the blood-CSF-barrier function on S100B in neurodegenerative diseases

Objectives - 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 - S100B(serum) and S100B(CSF) 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 (Q(alb)), which indicates the BCSFB functionality. Results - We reasserted increased S100B concentrations in CSF and serum of CJD patients. Elevated S100B(serum) correlated with elevated S100B(CSF) in all diagnoses but with exceptions. Neither S100B(CSF) nor S100B(serum) did correlate with Q(alb), even when the BCSFB function was progressively impaired as demonstrated by increased Q(alb). Conclusions - The lack of correlation between Q(alb) and S100B(CSF) 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.