Influence of the blood‐CSF‐barrier function on S100B in neurodegenerative diseases. (19th March 2013)

• Record Type: Journal Article
• Authors: Steinacker, P.; Weidehaas, K.; Cepek, L.; Feneberg, E.; Kretzschmar, H. A.; Otto, M.
• Is Part Of: Acta neurologica Scandinavica. Volume 128:Number 4(2013:Oct.)
• Page Start: 249
• Page End: 256
• Publication Date: 2013-03-19
• Subjects: albumin quotient -- blood‐cerebrospinal fluid barrier -- cerebrospinal fluid flow -- Creutzfeldt‐Jakob disease -- S100B; Neurology -- Periodicals; 616.8
• DOI: 10.1111/ane.12113
• Languages: English
• ISSNs: 0001-6314

Abstract

Abstract : 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: 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 ( Q alb ), which indicates the BCSFB functionality. Results: 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 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 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.