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


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 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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    ABSTRACT: Electroconvulsive therapy (ECT) is effective in treatment-resistant depression (TRD). It may act through intracellular process modulation, but its exact mechanism is still unknown. Animal research supports a neurotrophic effect for ECT. We aimed to investigate the association between changes in serum brain-derived neurotrophic factor (sBDNF) levels and clinical improvement following ECT in patients with TRD. Twenty-one patients with TRD (2 men, 19 women; mean age, 63.5 years; S.D., 11.9) were assessed through the Hamilton Depression Rating Scale (HDRS), the Brief Psychiatric Rating Scale (BPRS), and the Clinical Global Impressions scale, Severity (CGIs) before and after a complete ECT cycle. At the same time-points, patients underwent blood withdrawal for measuring sBDNF levels. ECT significantly reduced HDRS, BPRS, and CGIS scores, but not sBDNF levels. No significant correlation was found between sBDNF changes, and each of HDRS, BPRS, and CGIs score changes. sBDNF levels in TRD patients were low both at baseline and post-ECT. Our results do not support that improvements in TRD following ECT are mediated through increases in sBDNF levels. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
    04/2015; 227(2-3). DOI:10.1016/j.psychres.2015.04.009
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    • "However, as suggested by Yan et al. (2014), this point should be focused on, since functional effects of BDNF related to neurogenesis may require longer time to be observed. Fourth, despite differences between antidepressant drug classes in terms of mechanism of action and efficacy (Anderson, 1998; DUAG, 1990), and changes in BDNF serum levels (Matrisciano et al., 2009; Molendijk et al., 2011), no clinical study aimed at assessing the association between the effects of antidepressant classes and the BDNF Val66Met polymorphism on antidepressant efficacy. Yet no study has tested the impact of the BDNF Val66Met polymorphism on antidepressant efficacy, comparing different antidepressant drugs, with a sufficient study duration in Caucasian depressed patients. "
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    ABSTRACT: BACKGROUND: Whether the Brain Derived Neurotrophic Factor (BDNF) Val66Met polymorphism can predict antidepressant drug efficacy in depressed patients remains unclear, suggesting that it may depend on antidepressant classes. We assessed the impact of Val66Met polymorphism on antidepressant response and remission depending on antidepressant classes. METHODS: In a 6-month prospective, real-world setting, treatment study, 345 Caucasian depressed patients requiring a new or different drug treatment with a selective serotonin reuptake inhibitor (SSRI), a serotonin and noradrenalin reuptake inhibitor (SNRI) or a tricyclic antidepressant (TCA), were genotyped and assessed for response and remission. RESULTS: 231 (67%) patients were homozygous for the Val66 allele (Val/Val) and 114 (33%) were carriers of Met allele (Met). 152 (44.1%) patients were treated with SSRI, the others with SNRI/TCA. Both response and remission were explained by interactions between the Val66Met polymorphism and antidepressant drug classes (multivariate models adjusted for propensity-scores: p=0.02 and p=0.03 respectively). With SSRI, Val/Val patients had a higher response rate 3 months post-treatment than Met patients (68.1% versus 44%; adjusted-OR: 3.04, IC95% [1.05; 9.37], p=0.04). With SNRI/TCA, Val/Val patients had a lower remission rate 6 months post-treatment than Met patients (33.3% versus 60.9%, adjusted-OR: 0.27, IC95% [0.09; 0.76], p=0.02). LIMITATIONS: Limited sample size. CONCLUSIONS: This study argues for a personalized prescription of antidepressants in Caucasian patients with major depressive disorder, based on the BDNF Val66Met polymorphism: SSRI should be preferred for Val/Val patients and SNRI/TCA for Met patients. Further studies are required to confirm these data.
    Journal of Affective Disorders 04/2015; 175C:233-240. DOI:10.1016/j.jad.2015.01.013 · 3.38 Impact Factor
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    • "BDNF is a protein mostly expressed in the central nervous system and has an importance in survival and maintenance of neuronal functioning (Binder and Scharfman, 2004). Indeed, low neurotrophic activity has been seen as a mechanism underlying reduced cell numbers in the frontal cortex (Cotter et al., 2001; Rajkowska et al., 2001), and the amygdala (Bowley et al., 2002; Hamidi et al., 2004) and also underlying hippocampal volume (Videbech and Ravnkilde, 2004; Campbell et al., 2004), thus indicating that nerve growth factors, and more specifically, changes in BDNF, may play a crucial role in the development of and recovery from MDD (Castr en 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-Mill as et al., 2011; Mikoteit et al., 2014). In this context, Guilloux et al. (2012) were able to show reduced BDNF function in the amygdala of females suffering from MDD. "
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    ABSTRACT: Background: To treat patients suffering from treatment-resistant major depressive disorder (TR-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. Bdnf methods: 60 patients with TR-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 30 min, three times a week. Both depression severity and BDNF levels were assessed at baseline and 4 weeks later. All patients were further treated with an SSRI standard medication. Results: BDNF levels increased over time in all three study conditions. After completion of the intervention program, the ECT group showed significantly higher BDNF levels compared to the ECT + AET and the AET conditions. Depressive symptoms decreased in all three conditions over time. The combination of ECT + AET led to a significantly greater decrease 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 treatment patients suffering from TR-MDD, and that it remains unclear to what extent BDNF is key and a reliable biomarker for TR-MDD.
    Journal of Psychiatric Research 10/2014; 57(1). DOI:10.1016/j.jpsychires.2014.06.018 · 3.96 Impact Factor
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