Brain-derived neurotrophic factor (BDNF) changes in the serum of depressed women

Aydemir, Çiğdem; Yalçin, Esra; Aksaray, Sebahat; Kısa, Cebrail; Yildirim, Sema Gulen; Uzbay, Tayfun; Göka, Erol

doi:10.1016/j.pnpbp.2006.03.025

Cited by 193 publications

(138 citation statements)

References 34 publications

Supporting

Mentioning

125

Contrasting

Unclassified

Order By: Relevance

“…Thus, it is feasible that cytokine-induced decreases in BDNF may result in the depressogenic effects of inflammatory cytokines such as IFN-a. Consistent with this, several studies have associated low serum BDNF with MDD (Aydemir et al, 2006;BocchioChiavetto et al, 2006;Gervasoni et al, 2005;Hashimoto, 2010;Sen et al, 2008;Shimizu et al, 2003;Verhagen et al, 2010), which subsequently normalizes with antidepressant treatment (Castren and Rantamaki, 2010;Chen et al, 2001). Also, a functional polymorphism causing a change from valine (Val) to methionine (Met) may result in diminished BDNF secretion (Egan et al, 2003).…”

Section: Introductionmentioning

confidence: 85%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

View full text Add to dashboard Cite

Depression has been associated with inflammation, and inflammation may both influence and interact with growth factors such as brainderived neurotrophic factor (BDNF). Both the functional Val66Met BDNF polymorphism (rs6265) and BDNF levels have been associated with depression. It is thus plausible that decreased BDNF could mediate and/or moderate cytokine-induced depression. We therefore prospectively employed the Beck Depression Inventory-II (BDI-II), the Hospital Anxiety and Depression Scale (HADS), and the Montgomery-Asberg Depression Rating Scale (MADRS) in 124 initially euthymic patients during treatment with interferon-alpha (IFN-a), assessing serum BDNF and rs6265. Using mixed-effect repeated measures, lower pretreatment BDNF was associated with higher depression symptoms during IFN-a treatment (F 144,17.2 ¼ 6.8; Po0.0001). However, although the Met allele was associated with lower BDNF levels (F 1,83.0 ¼ 5.0; P ¼ 0.03), it was only associated with increased MADRS scores (F 4,8.9 ¼ 20.3; Po0.001), and not the BDI-II or HADS. An exploratory comparison of individual BDI-II items indicated that the Met allele was associated with suicidal ideation, sadness, and worthlessness, but not neurovegetative symptoms. Conversely, the serotonin transporter promoter polymorphism (5-HTTLPR) short allele was associated with neurovegetative symptoms such as insomnia, poor appetite and fatigue, but not sadness, worthlessness, or suicidal ideation. IFN-a therapy further lowered BDNF serum levels (F 4,37.7 ¼ 5.0; P ¼ 0.003), but this decrease occurred regardless of depression development. The findings thus do not support the hypothesis that decreasing BDNF is the primary pathway by which IFN-a worsens depression. Nonetheless, the results support the hypothesis that BDNF levels influence resiliency against developing inflammatory cytokine-associated depression, and specifically to a subset of symptoms distinct from those influenced by 5-HTTLPR. Neuropsychopharmacology (2013) 38, 985-995;

show abstract

Section: Introductionmentioning

confidence: 85%

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…There is also clinical evidence that antidepressants augment trophic factors in humans. For example, several studies report that depressed patients chronically treated with antidepressants have significantly higher plasma BDNF levels compared with non-treated subjects (Gonul et al, 2005;Aydemir et al, 2006). Furthermore, post-mortem studies confirm elevated BDNF expression in the dentate gyrus, hilus, and supragranular regions in patients treated with antidepressants compared with untreated patients (Chen et al, 2001).…”

Section: Introductionmentioning

confidence: 97%

Chronic Amitriptyline Treatment Attenuates Nigrostriatal Degeneration and Significantly Alters Trophic Support in a Rat Model of Parkinsonism

Paumier

Sortwell

Madhavan

et al. 2014

Neuropsychopharmacol

View full text Add to dashboard Cite

In addition to alleviating depression, long-term adaptive changes induced by antidepressants may regulate neural plasticity in the diseased brain, providing symptomatic and disease-modifying effects in Parkinson's disease. The present study investigated whether chronic treatment with a frequently prescribed tricyclic antidepressant was neuroprotective in a 6-hydroxydopamine (6-OHDA) rat model of parkinsonism. In lesioned animals, chronic amitriptyline (AMI; 5 mg/kg) treatment resulted in a significant sparing of tyrosine hydroxylaseimmunoreactive (THir) neurons in the substantia nigra pars compacta (SNpc) compared with saline treatment. Additionally, striatal fibers were preserved and functional motor deficits were attenuated. Although 6-OHDA lesions did not induce anhedonia in our model, the dose of AMI utilized had antidepressant activity as demonstrated by reduced immobility. Recent in vitro and in vivo data provide evidence that trophic factors such as brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) may be key mediators of the therapeutic response to antidepressants. Therefore, we investigated whether AMI mediates changes in these specific trophic factors in the intact and degenerating nigrostriatal system. Chronic AMI treatment mediates an increase in nigral BDNF both before and during ongoing degeneration, suggesting it may contribute to neuroprotection observed in vivo. However, over time, AMI reduced BDNF levels in the striatum, indicating tricyclic therapy differentially regulates trophic factors within the nigrostriatal system. Combined, these results suggest that AMI treatment attenuates dopamine neuron loss and elicits significant trophic changes relevant to dopamine neuron survival.

show abstract

“…Sensitivity Analysis -Serum BDNF and Depression Status Study Recalculated P value Table 4 Sensitivity Analysis -Serum BDNF and Antidepressant Treatment Study Recalculated P value Huang (47) 0.002 Piccinni (19) 0.013 Yoshimura (18) 0.019 Aydemir -A (45) 0.016 Gervasoni (44) 0.013 Gonul (48) 0.029 Aydemir -B (46) 0.002 Hellweg (50) 0.004…”

mentioning

confidence: 99%

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Sen

Duman

Sanacora

2008

Biological Psychiatry

1,082

715

View full text Add to dashboard Cite

show abstract

Brain-derived neurotrophic factor (BDNF) changes in the serum of depressed women

Cited by 193 publications

References 34 publications

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Brain-Derived Neurotrophic Factor Serum Levels and Genotype: Association with Depression during Interferon-α Treatment

Chronic Amitriptyline Treatment Attenuates Nigrostriatal Degeneration and Significantly Alters Trophic Support in a Rat Model of Parkinsonism

Serum Brain-Derived Neurotrophic Factor, Depression, and Antidepressant Medications: Meta-Analyses and Implications

Contact Info

Product

Resources

About