Serum S100B Levels and Major Depressive Disorder: Its Characteristics and Role in Antidepressant Response

Abstract

ObjectiveS100B is a neurotrophic factor that is involved in neuroplasticity. Neuroplasticity is disrupted in depression; however, treatment with antidepressants can restore neuroplasticity. S100B has previously been used as a biological marker for neuropathology and neuroplasticity; therefore, in this study, we compared serum S100B levels in depressive patients to those of normal controls. In addition, we compared the serum S100B levels of antidepressant responders to those of nonresponders.MethodsThirty five normal controls and 59 depressive patients were enrolled in this study. Depressive patients entered a 6 week clinical trial that included treatment with antidepressants. The serum S100B levels and clinical assessments, which included Hamilton depression rating scores, were measured at baseline and after 6 weeks of treatment with antidepressants. The difference in the serum S100B levels between depressive patients and normal controls and between antidepressant responders and nonresponders was then compared.ResultsThere were no significant differences in the serum S100B levels of normal controls and depressive patients. In addition, 30 of the depressive patients responded to antidepressant treatment while 29 did not. Finally, the responders had significantly higher baseline serum S100B levels than the nonresponders.ConclusionThe results of this study suggest that the baseline serum S100B level is associated with the subsequent response to antidepressants. In addition, the high baseline serum S100B level that was observed in depressive patients may enhance neuroplasticity, which results in a favorable therapeutic response to antidepressants.

Higher S100B Levels Predict Persistently Elevated Anhedonia with Escitalopram Monotherapy Versus Antidepressant Combinations: Findings from CO-MED Trial

“…As previously reported, participants who did not provide plasma samples in CO-MED trial were younger and had lower use of statin medication than those who provided plasma samples at baseline, but did not differ on any other baseline clinical and sociodemographic features [12]. Additionally, as participation in the continuation-phase of CO-MED was censured for those participants with inadequate response [32], only acute-phase visits (baseline and weeks 1, 2, 4, 6, 8, 10, and 12) were included in this report. The CO-MED trial used broad inclusion and exclusion criteria, (fully listed at https://clinicaltrials.gov/ct2/show/NCT00590863) while recruiting from psychiatric and primary care clinics that were chosen to ensure adequate minority representation and a diverse participant group [32].…”

“…Data for this report were obtained from the CO-MED trial where participants (n = 665) were randomized after stratification for site to one of the following treatment arms: escitalopram plus placebo, bupropion sustained-release (SR) plus escitalopram, and venlafaxine extended-release (XR) plus mirtazapine [32]. The analytic sample of this report (n = 153) includes a sub-set of CO-MED trial participants who provided plasma samples at baseline as part of a separate add-on optional biomarker study that required an additional consent.…”

“…Additionally, as participation in the continuation-phase of CO-MED was censured for those participants with inadequate response [32], only acute-phase visits (baseline and weeks 1, 2, 4, 6, 8, 10, and 12) were included in this report. The CO-MED trial used broad inclusion and exclusion criteria, (fully listed at https://clinicaltrials.gov/ct2/show/NCT00590863) while recruiting from psychiatric and primary care clinics that were chosen to ensure adequate minority representation and a diverse participant group [32]. The trial was reviewed and approved by the Institutional Review Boards at UT Southwestern Medical Center at Dallas, the University of Pittsburgh Data Coordinating Center, each participating regional center, and all relevant clinics.…”

Blood–brain barrier dysfunction in brain diseases: Clinical experience

“…Moreover, the severity of depression was positively correlated with serum S100B levels and with treatment response following 4 weeks of treatment (Schroeter et al., 2002; Arolt et al., 2003). Of interest, another study reported similar baseline levels of serum S100B in depressed patients and in control groups, however, found higher baseline levels to be predictive for treatment response to antidepressants (Jang et al., 2008).…”

Neurobiology of Major Depressive Disorder

“…SB100B is a protein associated with MDD which is expressed and secreted by glial cells and other nonneural cell lineages implicated in synaptogenesis and neuronal survival [92]. A number of recent studies have observed that SB100B is increased in the hippocampus, serum, and cerebrospinal fluid of MDD patients, most likely reflecting a response of glial cells to neural damage (see [93] and references therein) and also that the basal levels of serum may predict the outcome of the therapeutic response to antidepressants [94]. …”