Serum brain-derived neurotrophic factor and glucocorticoid receptor levels in lymphocytes as markers of antidepressant response in major depressive patients: A pilot study

Rojas, Paulina S.; Fritsch, Rosemarie; Rojas, Romina; Jara, Pablo; Fiedler, Jenny L.

doi:10.1016/j.psychres.2011.04.032

Cited by 35 publications

(18 citation statements)

References 53 publications

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“…The differential effects of pro-serotonergic and pronoradrenergic drugs on BDNF expression in animal models, in addition to the differential trends in BDNF plasma levels in relation to clinical response (depending on the specific drug used) suggest that BDNF pathway modulation by drugs could depend on interactions between specific pharmacodynamics and differential neurobiological backgrounds of subgroups of patients within depressive syndromes, such as ER vs. ENR in our study (specularly, ENR to drugs with a pro-noradrenergic component, as observed in our study, could reflect similar neurobiological backgrounds of ER to pro-serotonergic drugs, as observed in other studies: [5,6]). In particular, duloxetine blocks the same extent the reuptake of NE and 5-HT at standard dose (e.g.…”

Section: Discussionsupporting

confidence: 83%

“…However, data focused on drugs with predominant pro-serotonergic effects-such as several members of Selective Serotonin Reuptake Inhibitors (SSRIs), low-dose (75-150 mg/day) venlafaxine (a Serotonin Norepinephrine Reuptake Inhibitors-SNRIscharacterized by dose-dependent effects, i.e., pro-serotonergic at low dose and pro-noradrenergic also at higher dose [3]), and tricyclics like amitriptyline (contaminated by heterogeneous pharmacodynamics [4] )-whereas data on BDNF increase seem to be more consistent for SSRIs but more conflicting for venlafaxine and tricyclics [1,2,[5][6][7][8][9]. Interestingly, some studies detected an increase in BDNF levels only in early responders to SSRIs or low dose venlafaxine (6 weeks treatment), while no variations were found in non-responders [5,6]. However, pro-serotonergic drugs, such as SSRIs and specific tricyclics seem to be more effective in BDNF pathway enhancing, while pronoradrenergic drugs, such as desipramine and reboxetine seem not to affect BDNF expression (or at most in a modest way) [10,11].…”

Section: Introductionmentioning

confidence: 99%

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BDNF plasma levels variations in major depressed patients receiving duloxetine

et al. 2014

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It has been frequently reported that brain-derived neurotrophic factor (BDNF) plays an important role in the pathophysiology of major depressive disorder (MDD). Objective of the study was to investigate BDNF levels variations in MDD patients during antidepressant treatment with duloxetine. 30 MDD patients and 32 healthy controls were assessed using Hamilton Depression Scale (HAM-D) and monitored for BDNF plasma levels at baseline, week 6 and week 12 of duloxetine treatment (60 mg/day) and at baseline, respectively. According to early clinical response to duloxetine (defined at week 6 by reduction >50 % of baseline HAM-D score), MDD patients were distinguished in early responders (ER) and early non-responders (ENR), who reached clinical response at week 12. Laboratory analysis showed significant lower baseline BDNF levels among patients compared to controls. During duloxetine treatment, in ENR BDNF levels increased, reaching values not significantly different compared to controls, while in ER BDNF levels remained nearly unchanged. Lower baseline BDNF levels observed in patients possibly confirm an impairment of the NEI stress-adaptation system and neuroplasticity in depression, while BDNF increase and normalization observed only in ENR might suggest differential neurobiological backgrounds in ER vs. ENR within the depressive syndrome.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

BDNF plasma levels variations in major depressed patients receiving duloxetine

et al. 2014

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“…After 6 weeks of SSRI treatment, median values of change of both total and phosphorylated CREB were greater in responders than in nonrespond-ers . A greater increase in phosphorylated CREB in responders was confirmed by other studies using different pharmacological or psychotherapeutic treatments (Koch et al 2002(Koch et al , 2009, but no variation was reported after venlafaxine treat-ment (Rojas et al 2011). Inconsistent findings were reported in regard to CREB1 mRNA variations after antidepressant treatment (increased, Belzeaux et al 2010, or decreased, Lai et al 2003Iga et al 2007, levels).…”

Section: Peripheral Biomarkersmentioning

confidence: 67%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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“…Some confounding factors such as depressive status, antipsychotic drugs, extrapyramidal symptoms, and tardive dyskinesia may affect the level of BDNF. [23,24] Another interesting finding is the gender difference. A similar finding was reported in our previous study in which it was found that TrkB levels in women were increased significantly during depression.…”

Section: Discussionmentioning

confidence: 97%