S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia
Rothermundt M, Ponath G, Glaser T, Hetzel G, Arolt V (2004)
Neuropsychopharmacology 29(5): 1004-1011.
Zeitschriftenaufsatz
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Autor*in
Rothermundt, M;
Ponath, G;
Glaser, ThorstenUniBi;
Hetzel, G;
Arolt, V
Einrichtung
Abstract / Bemerkung
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.
Stichworte
astrocytes;
neurons;
longitudinal studies;
psychopathology;
S100 proteins;
schizophrenia
Erscheinungsjahr
2004
Zeitschriftentitel
Neuropsychopharmacology
Band
29
Ausgabe
5
Seite(n)
1004-1011
ISSN
0893-133X
Page URI
https://pub.uni-bielefeld.de/record/2397919
Zitieren
Rothermundt M, Ponath G, Glaser T, Hetzel G, Arolt V. S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Neuropsychopharmacology. 2004;29(5):1004-1011.
Rothermundt, M., Ponath, G., Glaser, T., Hetzel, G., & Arolt, V. (2004). S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Neuropsychopharmacology, 29(5), 1004-1011. https://doi.org/10.1038/sj.npp.1300403
Rothermundt, M, Ponath, G, Glaser, Thorsten, Hetzel, G, and Arolt, V. 2004. “S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia”. Neuropsychopharmacology 29 (5): 1004-1011.
Rothermundt, M., Ponath, G., Glaser, T., Hetzel, G., and Arolt, V. (2004). S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Neuropsychopharmacology 29, 1004-1011.
Rothermundt, M., et al., 2004. S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Neuropsychopharmacology, 29(5), p 1004-1011.
M. Rothermundt, et al., “S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia”, Neuropsychopharmacology, vol. 29, 2004, pp. 1004-1011.
Rothermundt, M., Ponath, G., Glaser, T., Hetzel, G., Arolt, V.: S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. Neuropsychopharmacology. 29, 1004-1011 (2004).
Rothermundt, M, Ponath, G, Glaser, Thorsten, Hetzel, G, and Arolt, V. “S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia”. Neuropsychopharmacology 29.5 (2004): 1004-1011.
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Schroeter ML, Abdul-Khaliq H, Fruhauf S, Hohne R, Schick G, Diefenbacher A, Blasig IE., Schizophr. Res. 62(3), 2003
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Selemon LD, Goldman-Rakic PS., Biol. Psychiatry 45(1), 1999
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Selemon LD, Goldman-Rakic PS., Biol. Psychiatry 45(1), 1999
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A review of MRI findings in schizophrenia.
Shenton ME, Dickey CC, Frumin M, McCarley RW., Schizophr. Res. 49(1-2), 2001
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Double-blind comparison of olanzapine versus risperidone in the treatment of schizophrenia and other psychotic disorders.
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Neurotoxicity, neuroplasticity, and magnetic resonance imaging morphometry: what is happening in the schizophrenic brain?
Weinberger DR, McClure RK., Arch. Gen. Psychiatry 59(6), 2002
PMID: 12044198
Weinberger DR, McClure RK., Arch. Gen. Psychiatry 59(6), 2002
PMID: 12044198
Transgenic mice overexpressing the neurotrophic factor S-100 beta show neuronal cytoskeletal and behavioral signs of altered aging processes: implications for Alzheimer's disease and Down's syndrome.
Whitaker-Azmitia PM, Wingate M, Borella A, Gerlai R, Roder J, Azmitia EC., Brain Res. 776(1-2), 1997
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Whitaker-Azmitia PM, Wingate M, Borella A, Gerlai R, Roder J, Azmitia EC., Brain Res. 776(1-2), 1997
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Elevated plasma levels of S-100b protein in schizophrenic patients.
Wiesmann M, Wandinger KP, Missler U, Eckhoff D, Rothermundt M, Arolt V, Kirchner H., Biol. Psychiatry 45(11), 1999
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Wiesmann M, Wandinger KP, Missler U, Eckhoff D, Rothermundt M, Arolt V, Kirchner H., Biol. Psychiatry 45(11), 1999
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Learning and memory in S100-beta transgenic mice: an analysis of impaired and preserved function.
Winocur G, Roder J, Lobaugh N., Neurobiol Learn Mem 75(2), 2001
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Winocur G, Roder J, Lobaugh N., Neurobiol Learn Mem 75(2), 2001
PMID: 11222062
Is schizophrenia a progressive neurodevelopmental disorder? Toward a unitary pathogenetic mechanism.
Woods BT., Am J Psychiatry 155(12), 1998
PMID: 9842773
Woods BT., Am J Psychiatry 155(12), 1998
PMID: 9842773
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