Pharmacopsychiatry 2005; 38 - A199
DOI: 10.1055/s-2005-918821

Glial cell dysfunction in schizophrenia indicated by increased S100B in the CSF

M Rothermundt 1, P Falkai 2, G Ponath 1, S Abel 1, M Diedrich 1, G Hetzel 1, M Peters 1, A Siegmund 1, W Maier 3, J Schramm 3, T Suslow 1, P Ohrmann 1, V Arolt 1
  • 1Universitätsklinikum Münster, Klinik für Psychiatrie, Münster
  • 2Klinik für Psychiatrie und Psychotherapie, Universität des Saarlandes, Homburg (Saar)
  • 3Klinik für Psychiatrie und Psychotherapie der Universität Bonn

Aims: Evidence from post mortem and MRI studies suggests that a dysfunction of glia cells might represent a pathogenic factor for schizophrenia. The astrocytic protein S100B regulates the balance between proliferation and differentiation in neurons and glia cells by modulating protective and apoptotic mechanisms. It therefore represents a marker for glial cell dysfunction, and has been shown to be increased in schizophrenia. However, until now only serum concentrations of S100B have been reported on in schizophrenic patients. This study represents the first attempt to study CSF and serum S100B concentrations in schizophrenia simultaneously.

Methods: S100B CSF and serum levels were examined in 21 unmedicated (including 16 drug naive first episode patients) schizophrenic patients and 21 age- and sex-matched healthy controls. Albumin and IgG CSF/ serum ratios were calculated to assess blood_brain-barrier (BBB) function.

Results: CSF and serum S100B concentrations were significantly increased in schizophrenics compared to healthy controls. The CSF/serum ratio was normal (20: 1). No BBB dysfunction was detected. There was a positive correlation between the severity of psychopathology and S100B serum levels.

Conclusion: Increased serum S100B concentrations reflect elevated CSF S100B levels in schizophrenic patients. These data provide further evidence that a dysfunction of glia cells might present a pathogenic factor in schizophrenia.