S100B and response to treatment in major depression: a pilot study

被引:96
作者
Arolt, V
Peters, M
Erfurth, A
Wiesmann, M
Missler, U
Rudolf, S
Kirchner, H
Rothermundt, M
机构
[1] Univ Munster, Dept Psychiat, D-48129 Munster, Germany
[2] Med Univ Lubeck, Dept Neuroradiol, D-23538 Lubeck, Germany
[3] Med Univ Lubeck, Inst Immunol & Transfus Med, D-23538 Lubeck, Germany
关键词
major depression; S100B; neuroprotection; neuroplasticity; response; antidepressant; ANTIDEPRESSANT TREATMENT; SCHIZOPHRENIC-PATIENTS; SEROTONERGIC NEURONS; NEUROTROPHIC FACTOR; CELL-PROLIFERATION; RAT HIPPOCAMPUS; PROTEIN; PREDICTION; NEUROGENESIS; ETHANOL;
D O I
10.1016/S0924-977X(03)00016-6
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
S100B is a protein which exerts both detrimental and neurotrophic effects, depending on its concentration in brain tissue. An increase of S100B in micromolar concentrations is observed in traumatic brain conditions and is associated with poor outcome. Micromolar levels of extracellular S100B in vitro may have deleterious effects. However, in nanomolar concentrations S100B has multiple neurotrophic effects in vitro may in vivo be regarded as a hallmark of neuroprotective efforts. This pilot study addresses the hypothesis that S100B serum concentrations may be of predictive validity for the response to antidepressant treatment in patients with major depression. S100B plasma levels were determined in 25 patients with major depression and 25 matched healthy controls using an immunofluorimetric sandwich assay. S100B plasma levels were significantly higher in major depressive patients than in healthy controls and positively correlated with treatment response after 4 weeks of treatment. In a linear regression model, a significant predictive effect was found only for S100B and severity of depressive symptoms upon admission. These results suggest that neuroprotective functions of S100B counterbalance neurodegenerative mechanisms that are involved in the pathophysiology of major depression and in the response to antidepressant treatment. (C) 2003 Elsevier B.V./ECNP. All rights reserved.
引用
收藏
页码:235 / 239
页数:5
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