Neuron-specific enolase is unaltered whereas S100B is elevated in serum of patients with schizophrenia - Original research and meta-analysis
Queen-Elisabeth-Hospital, Department of Psychiatry, 10362 Berlin, Germany. Psychiatry Research
(Impact Factor: 2.47).
05/2009; 167(1-2):66-72. DOI: 10.1016/j.psychres.2008.01.002
Previous studies reported altered levels of the astrocytic marker S100B in schizophrenia. To clarify mechanisms, we measured weekly serum levels of S100B together with the neuronal marker neuron-specific enolase in 20 patients with schizophrenia and 19 age- and gender-matched control subjects. S100B was elevated at admission and discharge in schizophrenic patients compared with control subjects, whereas there were no significant differences for neuron-specific enolase. Treatment had no impact on either S100B or neuron-specific enolase. A systematic, quantitative meta-analysis of all published studies involving 380 patients and 358 control subjects revealed elevated serum S100B in schizophrenia without any effect of antipsychotic treatment. Results suggest that increases of serum S100B are related to active secretion of S100B by astrocytes in combination with blood-brain barrier dysfunction in schizophrenia.
Available from: Meng Xia
- "When two markers of astroglial activation (myo-inositol and S100β) were assessed by 1 H-MRS or quantitative immunoassay, respectively, patients with increased S100β levels also had elevated concentrations of myo-inositol, suggesting a general dysfunction of glial cells not restricted to the specific astrocytic protein (i.e., S100β) (Rothermundt et al., 2007). A recent meta-analysis has revealed elevated serum S100β in schizophrenia without any effects of antipsychotics and has proposed that this increase is related to active secretion of the protein by astrocytes in combination with blood–brain barrier dysfunction in schizophrenia (Schroeter et al., 2009). However, there have been negative studies as well (Uzbay et al, 2013; van der Leeuw et al., 2013). "
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ABSTRACT: Astrocytes regulate multiple processes in the brain ranging from trophic support of developing neurons to modulation of synaptic neurotransmission and neuroinflammation in adulthood. It is, therefore, understandable that pathogenesis and pathophysiology of major psychiatric disorders involve astrocyte dysfunctions. Until recently, there has been the paucity of experimental approaches to studying the roles of astrocytes in behavioral disease. A new generation of in vivo models allows us to advance our understanding of the roles of astrocytes in psychiatric disorders. This review will evaluate the recent studies that focus on the contribution of astrocyte dysfunction to behavioral alterations pertinent to schizophrenia and will propose the possible solutions of the limitations of the existing approaches.
Available from: Stefania Boccia
- "During the last twenty years the S100B protein has gained attention in the research area for peripheral biomarkers of schizophrenia [ 66 ] . We carried out a meta - analysis including both the studies considered in those of Schroeter et al . , 2009 [ 23 , 24 ] and seven new studies [ 39 , 40 , 45 , 51 , 52 , 53 , 55 ] . Our results confirmed the in - creased S100B values in cases than controls found by Schroeter et al ; in addition , we could carry out sensitivity and stratified analyses in order to assess the presence of confounding factors and effect modifiers . Subgroups analys"
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ABSTRACT: S100B is a calcium-binding protein secreted in central nervous system from astrocytes and other glia cells. High blood S100B levels have been linked to brain damage and psychiatric disorders. S100B levels have been reported to be higher in schizophrenics than healthy controls. To quantify the relationship between S100B blood levels and schizophrenia a systematic literature review of case-control studies published on this topic within July 3rd 2014 was carried out using three bibliographic databases: Medline, Scopus and Web of Science. Studies reporting mean and standard deviation of S100B blood levels both in cases and controls were included in the meta-analysis. The meta-Mean Ratio (mMR) of S100B blood levels in cases compared to controls was used as a measure of effect along with its 95% Confidence Intervals (CI). 20 studies were included totaling for 994 cases and 785 controls. Schizophrenia patients showed 76% higher S100B blood levels than controls with mMR = 1.76 95% CI: 1.44-2.15. No difference could be found between drug-free patients with mMR = 1.84 95%CI: 1.24-2.74 and patients on antipsychotic medication with mMR = 1.75 95% CI: 1.41-2.16). Similarly, ethnicity and stage of disease didn't affect results. Although S100B could be regarded as a possible biomarker of schizophrenia, limitations should be accounted when interpreting results, especially because of the high heterogeneity that remained >70%, even after carrying out subgroups analyses. These results point out that approaches based on traditional categorical diagnoses may be too restrictive and new approaches based on the characterization of new complex phenotypes should be considered.
Available from: Jogin Thakore
- "While some studies have reported the levels of S100B to be altered dependent on medication, these reports have been contradictory
[31,33,35,41-44]. Furthermore, little is known about the direct effects of antipsychotic medication on glial cells within the central nervous system. "
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The neurotrophic factor, S100B, is released primarily from astrocytes, with serum and CSF levels of S100B reported as altered in schizophrenia. However, many of these reports are contradictory. Here, serum levels of S100B in schizophrenia and influence of age, gender, medication and illness severity were examined.
Serum S100B levels were measured in patients with schizophrenia treated with clozapine. Lifestyle, metabolic and illness severity parameters were correlated with S100B concentrations.
Data showed raised serum levels of S100B in schizophrenia female patients, but not male patients, compared to controls. Correlation analysis demonstrated a positive association between S100B serum concentrations and BMI.
This study supports previous findings that adipocytes may contribute to S100B serum concentrations in females, in addition to astrocytes. This study also supports the hypothesis that metabolic effects of medication, lifestyle choices and the illness itself, may be contributing factors to altered levels of S100B.
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