Elevated plasma levels of S-100b protein in schizophrenic patients

Wiesmann, Martin; Wandinger, Klaus Peter; Mißler, U.; Eckhoff, Dörte; Rothermundt, Matthias; Arolt, Volker; Kirchner, Holger

doi:10.1016/s0006-3223(98)00217-0

Cited by 96 publications

(76 citation statements)

References 22 publications

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“…This hypothesis may explain the higher serum levels of S100B in medicated patients in comparison with unmedicated patients and healthy controls in our study, particularly because the majority of patients received typical antipsychotics. Thus, our results are in accordance with Wiesmann et al (1999) who showed elevated S100B levels in medicated schizophrenic patients compared with healthy controls.…”

Section: Discussionsupporting

confidence: 93%

“…Thus, one may hypothesize that antipsychotics increase S100B during the first weeks of treatment, whereas in the long run, after more than 5 weeks, they decrease S100B, at least in patients with a small amount of negative symptoms. According to this hypothesis, Wiesmann et al (1999) and our study measured elevated S100B during the first weeks of treatment, whereas Gattaz et al (2000) and Rothermundt et al (2001) measured decreased levels of S100B after more than 5 weeks of treatment, at least in patient subgroups.…”

Section: Discussionmentioning

confidence: 50%

“…However, the impact of antipsychotic medication on S100B is controversial. Increased (Wiesmann et al, 1999) and decreased levels (Gattaz et al, 2000) of S100B were reported in medicated schizophrenic patients in comparison with healthy controls. Further, Rothermundt et al (2001) showed that treatment with antipsychotics for 6 weeks reduced S100B in this subgroup of patients, which had less negative symptoms, whereas S100B was unchanged in the subgroup with more negative symptoms at admission and after 6 weeks treatment.…”

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confidence: 97%

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Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia

Schroeter

Abdul‐Khaliq

Frühauf

et al. 2003

Schizophrenia Research

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Previous studies reported controversial results concerning alterations of astrocytes in schizophrenia. Because S100B may be regarded as a marker for astrocytes, the objective of this study was to examine S100B serum concentrations in 30 patients with schizophrenia with a monoclonal two-site immunoluminometric assay that specifically detects S100B. An ANOVA revealed medication ( p < 0.005) and deficit vs. nondeficit syndrome ( p < 0.05) as factors that influenced S100B significantly. S100B was higher in schizophrenic patients treated with antipsychotic drugs for approximately 3 weeks (241.1 F 152.5 ng/l) in comparison with unmedicated patients (111.4 F 31.8 ng/l, p < 0.005), and healthy age-matched controls (112.8 F 53.4 ng/l, p < 0.001; Bonferroni corrected two-tailed Student's t-test). There was no difference of S100B between unmedicated patients and controls ( p>0.05). Patients with deficit (250.6 F 154.9 ng/l) had higher S100B levels than patients with nondeficit schizophrenia (146.7 F 107.2 ng/l, p < 0.05) or controls ( p < 0.005). S100B was positively correlated with the subscore 'thought disturbance' of the Brief Psychiatric Rating Scale ( p < 0.05). In summary, increased serum levels of S100B may indicate alterations of astrocytes during early treatment with antipsychotics and in deficit schizophrenia. Whether S100B is elevated due to injured astrocytes and a disrupted blood -brain barrier, or by active secretion of S100B by astrocytes, has to be clarified by further studies. D

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 50%

mentioning

confidence: 97%

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Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia

Schroeter

Abdul‐Khaliq

Frühauf

et al. 2003

Schizophrenia Research

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“…About 40% of the schizophrenics showed S100B levels higher than the mean plus two SDs of the healthy control group at all investigation time points. Comparable numbers were reported earlier for an acute stage of disease (Lara et al, 2001;Rothermundt et al, 2001;Schroeter et al, 2003;Wiesmann et al, 1999). It appears that a subgroup of schizophrenic patients (about 40%) exhibits increased S100B levels that are relatively stable over time and which do not normalize after recovery from an acute episode.…”

Section: Discussionsupporting

confidence: 83%

“…In neurodegenerative and neuroinflammatory diseases, increased S100B levels may result from S100B secretion or release from damaged astrocytes. In schizophrenia, several studies have shown increased S100B serum levels in the acute stage of disease (Wiesmann et al, 1999;Lara et al, 2001;Rothermundt et al, 2001;Schroeter et al, 2003). Lara et al (2001) reported higher levels in patients with recent onset of disease compared to chronic patients while Rothermundt et al (2001) demonstrated that continuously increased S100B levels after 6 weeks are associated with negative symptomatology.…”

Section: Introductionmentioning

confidence: 99%

S100B Serum Levels and Long-Term Improvement of Negative Symptoms in Patients with Schizophrenia

Rothermundt

Ponath

Gläser

et al. 2004

Neuropsychopharmacol

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104

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S100B, a calcium-binding protein produced by astroglial cells, mediates paracrine and autocrine effects on neurons and glial cells. It regulates the balance between proliferation and differentiation in neurons and glial cells by affecting protective and apoptotic mechanisms. Post-mortem studies have demonstrated a deficit in synapses and dendrites in brains of schizophrenics. Recent studies have shown increased S100B levels in medicated acutely psychotic schizophrenic patients as well as unmedicated or drug naive schizophrenics. One study reported a positive correlation between negative symptoms and S100B. S100B serum levels (quantitative immunoassay) and psychopathology (Positive and Negative Syndrome Scale, PANSS) were examined upon study admission and after 12 and 24 weeks of standardized treatment in 98 chronic schizophrenic patients with primarily negative symptoms. Compared to age-and sex-matched healthy controls, the schizophrenic patients showed significantly increased S100B concentrations upon admission and after 12 and 24 weeks of treatment. High PANSS negative scores were correlated with high S100B levels. Regression analysis comparing psychopathology subscales and S100B identified negative symptomatology as the predicting factor for S100B. S100B is not just elevated during acute stages of disease since it remains elevated for at least 6 months following an acute exacerbation. With regard to psychopathology, negative symptomatology appears to be the predicting factor for the absolute S100B concentration. This might indicate that S100B in schizophrenic patients either promotes apoptotic mechanisms by itself or is released from astrocytes as part of an attempt to repair a degenerative or destructive process.

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Functional assessment of a promoter polymorphism in S100B, a putative risk variant for bipolar disorder

Dağdan¹,

Morris²,

Campbell³

et al. 2011

American J of Med Genetics Pt B

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Calcium-binding protein S100B has been implicated in the pathology of bipolar affective disorder (BPAD) and schizophrenia (SZ). S100B protein levels are elevated in serum of patients with both disorders compared to controls. We previously reported genetic association of a SNP in the promoter of S100B, rs3788266, with a psychotic form of BPAD. To test for genotypic effects of rs3788266 in vivo, S100B serum protein levels were measured in 350 Irish and German subjects of known S100B genotype. The functional effect of rs3788266 on S100B promoter activity was studied using the luciferase reporter system in U373MG glioblastoma and SH-SY5Y neuroblastoma cell lines. Allelic effects of rs3788266 on protein complex formation at the S100B promoter were investigated by an electrophoretic mobility shift assay. Higher mean serum S100B levels were associated with the risk G allele of rs3788266 in BPAD cases (P = 0.0001), unaffected relatives of BPAD cases (P< 0.0001) and unrelated controls (P < 0.0001). Consistent with the in vivo findings, luciferase gene expression was significantly increased in the presence of the G allele compared to the A allele in SH-SY5Y (P = <0.0001), and in U373MG (P = <0.0008) cell lines. The binding affinity of both SH-SY5Y and U373MG protein complexes for the S100B promoter was significantly stronger in the presence of G allele compared to the A allele promoter fragments. These data support rs3788266 as a functional promoter variant in the S100B gene where the presence of the G allele promotes increased gene expression and is associated with increased serum levels of the protein.

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Elevated plasma levels of S-100b protein in schizophrenic patients

Cited by 96 publications

References 22 publications

Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia

Serum S100B is increased during early treatment with antipsychotics and in deficit schizophrenia

S100B Serum Levels and Long-Term Improvement of Negative Symptoms in Patients with Schizophrenia

Functional assessment of a promoter polymorphism in S100B, a putative risk variant for bipolar disorder

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