Serum S-100β as a possible marker of blood–brain barrier disruption

doi:10.1016/S0006-8993(02)02586-6

Brain Research

Volume 940, Issues 1–2, 14 June 2002, Pages 102-104

https://doi.org/10.1016/S0006-8993(02)02586-6 Get rights and content

Abstract

Two brain-specific proteins, S-100β and neuron-specific enolase (NSE), are released systemically after cerebral lesions, but S-100β levels sometimes rise in the absence of neuronal damage. We hypothesized that S-100β is a marker of blood–brain barrier (BBB) leakage rather than of neuronal damage. We measured both proteins in the plasma of patients undergoing iatrogenic BBB disruption with mannitol, followed by chemotherapy. Serum S-100β increased significantly after mannitol infusion (P<0.05) while NSE did not. This suggests that S-100β is an early marker of BBB opening that is not necessarily related to neuronal damage.

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Acknowledgements

This work was supported by NIH-2RO1 HL51614, NINDS RO1-43284 and NIH-RO1 NS38195 to DJ. SANGTEC Med. (Bromma, Sweden) provided antibodies for S-100β and NSE detection. We like to thank Dr. A-C Aronsson for helpful discussion. We would also like to thank Jessica Ancker for editing the manuscript.

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Citation Excerpt :
Within that context, and consistent with our hypothesis, serum S100B concentrations were elevated following SERE training, suggesting an increase in BBB permeability. Although S100B can be released from extracerebral sources (Koh and Lee, 2014), the brain appears to be the primary origin of circulating S100B (Anderson et al., 2001; Pham et al., 2010), and serum S100B concentrations are a strong indicator of the extent of BBB disruption measured using more direct methods such as magnetic resonance imaging (Kanner et al., 2003; Kapural et al., 2002; Yardan et al., 2011; Vogelbaum et al., 2005; Marchi et al., 2007; Marchi et al., 2003; Teepker et al., 2009). Indeed, serum S100B concentrations have been used as a diagnostic biomarker for brain injury, hypoxia exposure, dehydration, heat strain, and stress (Watson et al., 2006; Teepker et al., 2009; Diebel et al., 2005; Gerlach et al., 2006; Kleindienst et al., 2007; Scaccianoce et al., 2004; Watson et al., 2005).
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FFM, psychomotor vigilance, and LBP decreased from PRE to POST, while TMD, anxiety, and depression scores, and S100B, DHEA-S, IL-6, norepinephrine, and epinephrine concentrations all increased (all p ≤ 0.01). Increases in DHEA-S were associated with decreases in body mass (p = 0.015). Decreases in FFM were associated with decreases in LBP concentrations (p = 0.015), and both decreases in FFM and LBP were associated with increases in TMD and depression scores (all p < 0.05) but not with changes in cognitive performance. Conversely, increases in S100B concentrations were associated with decreases in psychomotor vigilance (p < 0.05) but not with changes in mood state or LBP concentrations.
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Short communicationSerum S-100β as a possible marker of blood–brain barrier disruption

Abstract

Section snippets

Acknowledgements

Brain Res.

Prog. Neurobiol.

J. Thorac. Cardiovasc. Surg.

Epilepsy Res.

J. Cardiothorac. Vasc. Anesth.

Adv. Virus Res.

Physiology and pathology of the blood–brain barrier: implications for microbial pathogenesis, drug delivery and neurodegenerative disorders

J. Neurovirol.

Down syndrome and the trisomy 16 mouse: impact of gene imbalance on brain development and aging

Res. Publ. Assoc. Res. Nerv. Ment. Dis.

Short communication
Serum S-100β as a possible marker of blood–brain barrier disruption