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J Neurol Neurosurg Psychiatry 2006;77:1284-1287 doi:10.1136/jnnp.2006.093427
  • Short report

Increased cerebrospinal fluid and serum levels of S100B in first-onset schizophrenia are not related to a degenerative release of glial fibrillar acidic protein, myelin basic protein and neurone-specific enolase from glia or neurones

  1. J Steiner1,
  2. H Bielau1,
  3. H-G Bernstein1,
  4. B Bogerts1,
  5. M T Wunderlich2
  1. 1Department of Psychiatry, University of Magdeburg, Magdeburg, Germany
  2. 2Department of Neurology, University of Magdeburg
  1. Correspondence to:
 J Steiner
 Department of Psychiatry, University of Magdeburg, Leipziger Strasse 44, D-39120 Magdeburg, Germany; johann.steiner{at}medizin.uni-magdeburg.de
  • Received 17 March 2006
  • Accepted 1 August 2006
  • Revised 17 July 2006

Abstract

Objective: To assess levels of glial fibrillar acidic protein (GFAP), myelin basic protein (MBP), neurone-specific enolase (NSE) and S100B in patients with first-onset schizophrenia.

Method: We investigated CSF and serum samples from 12 patients with first-onset schizophrenia and from 17 control subjects by ELISA (GFAP, MBP) or immunoluminometric sandwich assays (NSE, S100B).

Results: Patients with schizophrenia had significantly higher levels of S100B in CSF (p = 0.004; 2.73 (SD 0.80) v 1.92 (0.58) μg/l) and serum (p = 0.032; 0.09 (0.03) v 0.08 (0.02) μg/l) in comparison with those in the matched control group. No diagnosis-dependent differences of protein concentration were seen for GFAP, MBP and NSE.

Discussion: Our finding of increased levels of S100B in patients with schizophrenia without an indication for significant glial (GFAP, MBP) or neuronal (NSE) damage may be interpreted as indirect evidence for increased active secretion of S100B during acute psychosis.

Footnotes

  • Competing interests: None.

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