Partial Normalization of Serum Brain-Derived Neurotrophic Factor in Remitted Patients after a Major Depressive Episode
Department of Psychiatry, University of Geneva, Genève, Geneva, Switzerland Neuropsychobiology
(Impact Factor: 2.26).
02/2005; 51(4):234-8. DOI: 10.1159/000085725
We had previously reported decreased serum brain-derived neurotrophic factor (BDNF) levels in depressed patients. In the present study, we tested the hypothesis that antidepressant treatment would normalize serum BDNF levels, at least in a subgroup of patients. Major depressed patients (15 females and 11 males) diagnosed according to DSM-IV criteria and healthy controls (13 females and 13 males) participated in this study. Serum BDNF was assayed with the ELISA method for depressed and remitted patients and the severity of depression was evaluated with the Montgomery-Asberg Depression Rating Scale. An analysis of variance showed that treatment had an effect [F(1, 24) = 4.46, p = 0.045] on the normalization of serum BDNF levels. We also found a correlation between the severity of depression (r = 0.51, p = 0.008), the pretreatment BDNF levels (r = 0.62, p = 0.001) and the difference in serum BDNF levels after antidepressant treatment. These results suggest that antidepressant treatment has a positive effect on serum BDNF levels and support the hypothesis of neurotrophic factor involvement in affective disorders.
Available from: Undine E Lang
- "Upregulation of BDNF may reverse stress-induced deficits in structural and synaptic plasticity in the adult brain, resulting in cognitive flexibility and an increased ability to adapt with environmental challenges that may precipitate or exacerbate depressive episodes. Recent studies demonstrate that BDNF levels are decreased in the blood of depressed patients and its levels are increased with antidepressant treatment (Aydemir et al., 2005; Brunoni et al., 2008; Deuschle et al., 2013; Gervasoni et al., 2005; Karege et al., 2002; Kim et al., 2007; Lee et al., 2006, 2011; Ricken et al., 2013; Sen et al., 2008; Shimizu et al., 2003). Moreover, human BDNF polymorphism and serum levels have been connected with anxiety, risk of depression, neuroticism and serotonergic neurotransmission (Lang et al., 2002; 2004, 2005a, 2005b, 2007, 2009a, 2009b). "
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ABSTRACT: Major depression is a common, recurrent mental illness that affects millions of people worldwide. Recently, a unique fast neuroprotective and antidepressant treatment effect has been observed by ketamine, which acts via the glutamatergic system. Hence, a steady accumulation of evidence supporting a role for the excitatory amino acid neurotransmitter (EAA) glutamate in the treatment of depression has been observed in the last years. Emerging evidence indicates that N-methyl-D-aspartate (NMDA), group 1 metabotropic glutamate receptor antagonists and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) agonists have antidepressant properties. Indeed, treatment with NMDA receptor antagonists has shown the ability to sprout new synaptic connections and reverse stress-induced neuronal changes. Based on glutamatergic signaling, a number of therapeutic drugs might gain interest in the future. Several compounds such as ketamine, memantine, amantadine, tianeptine, pioglitazone, riluzole, lamotrigine, AZD6765, magnesium, zinc, guanosine, adenosine aniracetam, traxoprodil (CP-101,606), MK-0657, GLYX-13, NRX-1047, Ro25-6981, LY392098, LY341495, D-cycloserine, D-serine, dextromethorphan, sarcosine, scopolamine, pomaglumetad methionil, LY2140023, LY404039, MGS0039, MPEP, 1-Aminocyclopropanecarboxylic acid all of which target this system have already been brought up, some of them recently. Drugs targeting the glutamatergic system might open up a promising new territory for the development of drugs to meet the needs of patients with major depression.
Copyright © 2015. Published by Elsevier Inc.
- "Logistic regressions were run to examine the relationship between BDNF and remissions status. The model was adjusted for variables (age, gender, smoking, illness duration, antidepressant use, antipsychotic type and dosage) which were previously found to influence serum BDNF levels in an effort to minimise potentially confounding influence (Chen and Huang, 2011; Gervasoni et al., 2005; Green et al., 2011; Nurjono et al., 2012; Trajkovska et al., 2007; Wang et al., 2007; Xiu et al., 2009 "
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ABSTRACT: The neurotrophin, brain-derived neurotrophic factor (BDNF), characterises a probable neurobiochemical explanation of maldevelopments in schizophrenia and is a candidate biomarker of the illness. A paucity of studies examining neurobiochemical predictors of remission in schizophrenia exists. In this study, we seek to examine if serum BDNF level is associated with remission status in a sample of Chinese patients with schizophrenia. This study did not find a significant relationship between serum BDNF and remission in patients with schizophrenia. Identification of a suitable biomarker for diagnosis, management, and prognostic outcome is crucial and warrants further study.
Available from: Faezeh Vahdati Hassani
- "BDNF structurally belongs to the neurotrophin family that plays an important role in regulation of neuronal differentiation including neurotransmitter content and neuronal survival . Recent studies have shown that after treatment with antidepressants, levels of BDNF significantly increased in plasma [55,56]. It was evidenced that use of imipramine as a nonselective 5-HT and NE reuptake inhibitor at doses of 10 and 20 mg/kg was effective to increase BDNF protein levels in both prefrontal cortex and hippocampus . "
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ABSTRACT: Antidepressants have been shown to affect levels of brain-derived neurotrophic factor (BDNF) and VGF (non-acronymic) whose transcriptions are dependent on cAMP response element binding protein (CREB) in long term treatment. The aim of this study was to verify the subacute antidepressant effects of crocin, an active constituent of saffron (Crocus sativus L.), and its effects on CREB, BDNF, and VGF proteins, transcript levels and amount of active, phosphorylated CREB (P-CREB) protein in rat hippocampus.
Crocin (12.5, 25, and 50 mg/kg), imipramine (10 mg/kg; positive control) and saline (1 mL/kg; neutral control) were administered intraperitoneally (IP) to male Wistar rats for 21 days. The antidepressant effects were studied using the forced swimming test (FST) on day 21 after injection. Protein expression and transcript levels of genes in the rat hippocampus were evaluated using western blot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR), respectively.
Crocin significantly reduced the immobility time in the FST. Western blot analysis showed that 25 and 50 mg/kg of crocin increased the levels of CREB and BDNF significantly and dose dependently. All doses of crocin increased the VGF levels in a dose-dependent manner. Levels of p-CREB increased significantly by 50 mg/kg dose of crocin. Only 12.5 mg/kg crocin could significantly increase the transcript levels of BDNF. No changes in CREB and VGF transcript levels were observed in all groups.
These results suggest that crocin has antidepressant-like action by increasing CREB, BDNF and VGF levels in hippocampus.
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