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Changes in BDNF serum levels in patients with depression disorder (MDD) after 6 months treatment with sertraline, escitalopram, or venlafaxine

Department of Psychiatry and Psychological Medicine, University of Rome "La Sapienza" "Sant'Andrea" Hospital, Via di Grottarossa, 1035/1039, 00189 Rome, Italy.
Journal of Psychiatric Research (Impact Factor: 3.96). 06/2008; 43(3):247-54. DOI: 10.1016/j.jpsychires.2008.03.014
Source: PubMed

ABSTRACT

Recent studies have implicated brain-derived neurotrophic factor (BDNF) in the pathophysiology of depression and the activity of antidepressant drugs. Serum BDNF levels are lower in depressed patients, and increase in response to antidepressant medication. However, how BDNF responds to different classes of antidepressant drugs is unknown. We assessed serum BDNF levels in 21 patients with major depressive episode treated with sertraline, escitalopram, or venlafaxine and 20 healthy controls. Serum samples were collected between 10 a.m. and 12 p.m. at baseline, 5 weeks, and 6 months of treatment. BDNF levels were measured via immunoassay. The severity of symptoms and response to treatment were assessed by the Hamilton rating scales for depression (HRSD). Baseline serum BDNF levels were significantly lower in depressed patients compared to controls. Sertraline increased BDNF levels after 5 weeks and 6 months of treatment. Venlafaxine increased BDNF levels only after 6 months. Escitalopram did not affect BDNF levels at either time point. A significant negative association was found between percentage increase in BDNF levels and percentage decreased in HRSD scores after 6 months of treatment. In conclusion, these results suggest that different antidepressant drugs have variable effects on serum BDNF levels. This is true even though the three different drugs were equally effective in relieving symptoms of depression and anxiety.

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Available from: Angelo Ricciardi, May 18, 2014
    • "The present findings, however, are also in accord with studies in which no association between symptom improvement and BDNF levels was found (Toups et al. 2011;Gedge et al. 2012;Fernandez et al. 2009;GrØnli 2009;Bocchio-Chiavetto et al. 2006), but is at odds with others which claim that symptom improvements and increasing BDNF levels are associated (cf.Siuciak et al. 1997;Shirayama et al. 2002). Thus, even if it is accepted that BDNF can play a crucial role in the development of and recovery from MDD (Castrén et al. 2007;Karege et al. 2002;Sen et al. 2008;Molendijk et al. 2011;Sen et al., 2008;Guilloux et al., 2012;Wolkowitz et al., 2011, Matrisciano et al., 2009, Serra-Millàs et al., 2011Mikoteit et al, 2014), we would also note that symptom improvements and BDNF levels appear to be unrelated (cf.Brunoni et al., 2014). In this respect, importantly,Sen et al. (2008)concluded from a meta-analysis that BDNF-levels are lower in people suffering from MDD than in controls, and followingHasselbalch et al (2012)this also holds true when patients are fully remitted. "
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    ABSTRACT: Background: To treat patients suffering from major depressive disorder (MDD), research has focused on electroconvulsive therapy (ECT) and aerobic exercise training (AET). Brain derived neurotrophic factor (BDNF) seems to be key in MDD. The aims of the present study were therefore two-fold, to investigate in a three-arm interventional study the differential effects of ECT, ECT plus AET, and AET alone in patients suffering from TR-MDD on 1. depressive symptoms and 2. plasma BDNF (pBDNF). Methods: 60 patients with MDD (mean age: 31 years; 31.6% female patients) were randomly assigned either to the ECT, ECT + AET, or AET condition. The AET condition consisted of treadmill exercise for 45 min, three times a week. Both depression severity and pBDNF levels were assessed at baseline and 4 weeks later. All patients were further treated with an SSRI standard medication. Results: pBDNF levels increased over time in all three study conditions, though, highest increase was observed in the ECT + EAT condition, and lowest increase was observed in the AET condition. Depressive symptoms decreased in all three conditions over time, though, strongest decrease was observed in the ECT + AET condition. The combination of ECT + AET led to significantly greater remission rates than in either the ECT or AET alone conditions. BDNF levels were not associated with symptoms of depression. Conclusions: The pattern of results suggests that ECT, AET and particularly their combination are promising directions for the treatment of patients suffering from MDD, and that it remains unclear to what extent pBDNF is key and a reliable biomarker for MDD.
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    • "The activation of TrkB facilitates neuronal survival, differentiation and synaptogenesis[35,36], whereas p75 NTR triggers apoptosis[37,38]. BDNF is reduced in patients with MDD and AD39404142, but can be rescued by antidepressant intervention[43,44]and anti-dementia drugs[45]. We have reported that microglial hyper-activation suppresses astrocyte-mediated neurotrophin functions and induces neurodegeneration[29]. "
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    • "The main finding of this study was that changes in sBDNF levels did not correlate with changes in depression severity. Baseline sBDNF levels in our TRD sample were lower than commonly reported normal values (Lang et al., 2004), which matches previous data (Karege et al., 2002; Lee et al., 2007; Matrisciano et al., 2009; Wolkowitz et al., 2011), and supports the hypothesis of neurotrophic factor deficits in the pathogenesis of TRD (Sen et al., 2008). Some studies reported a negative correlation of sBDNF levels with the severity of depression (Karege et al., 2002; Gonul et al., 2005). "
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