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Treatment response in major depression is correlated with an increased concentration of the neuroplasticity marker S100B
Objective: Recent evidence suggests that neurodegenerative mechanisms may be involved in the pathophysiology of major depression. Structural and functional changes might be caused by alterations of dendrites and synapses. The astroglial protein S100B regulates the balance between proliferation and differentiation in neurons and glial cells affecting protective and apoptotic mechanisms. Two earlier studies reported increased S100B CSF and serum levels in acutely depressed patients.
Methods: In 25 patients suffering from major depression (CIDI) psychopathology (HAMD) and S100B serum levels (immunofluorimetric sandwich assay) were investigated in an acute stage and after 4 weeks of treatment.
Results: The mean S100B serum concentration was significantly increased in depressed patients compared to healthy controls. The relative response rate to antidepressant therapy after 4 weeks correlated positively with S100B levels. In a regression analysis, only S100B concentrations and HAMD total score predicted the therapeutic response.
Conclusion: Neuroprotective functions of S100B might positively influence therapy response in depression.
Rothermundt M, Arolt V, Wiesmann M, Missler U, Peters M, Rudolf S, Kirchner H:
S-100B is increased in melancholic but not in non-melancholic major depression.
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Grabe HJ, Ahrens N, Rose HJ, Kessler C, Freyberger HJ: Neurotrophic factor s100beta in major depression. Neuropsychobiol 44 (2001) 88–90
Arolt V, Peters M, Erfurth A, Wiesmann M, Missler U, Rudolf S, Kirchner H, Rothermundt M: S100B and response to treatment in major depression: A pilot study. Eur Neuropsychopharmacol 2003 in press