Decreased serum brain-derived neurotrophic factor (BDNF) is associated with post-stroke depression but not with<i>BDNF</i>gene Val66Met polymorphism

Zhou, Zhiming; Lü, Tingting; Xu, Guiping; Yue, Xuanye; Zhu, Wenhui; Ma, Minmin; Liu, Wenhua; Zhu, Shuanggen; Liu, Xinfeng

doi:10.1515/cclm.2011.039

Cited by 70 publications

(60 citation statements)

References 35 publications

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“…However, acknowledging the small effect sizes we found, this latter study could have been underpowered. Secondly, differences in the association between Val66Met and serum BDNF levels could further be explained by differences in psychopathology, as two studies included depressed subjects [9,11] and race, and two studies were carried out in Asian populations [9,10,11], whereas others included Caucasians [7,8]. …”

Section: Discussionmentioning

confidence: 99%

“…Genetic association studies, however, have yielded conflicting results, as higher [7,8], lower [9] and similar [10,11] BDNF levels in Met allele carriers of the Val66Met polymorphism were shown. Inconsistencies may be explained by psychopathology, race and/or gender.…”

Section: Introductionmentioning

confidence: 99%

“…Inconsistencies may be explained by psychopathology, race and/or gender. First, two studies investigating the relationship between genotype and serum BDNF levels were performed in depressed subjects [9,11]; others were performed in healthy subjects [7,8,10]. Secondly, two studies were carried out in Asian populations [10,11]; others comprised Caucasians only [7,8,9].…”

Section: Introductionmentioning

confidence: 99%

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Increase in Serum Brain-Derived Neurotrophic Factor in Met Allele Carriers of the BDNF Val66Met Polymorphism Is Specific to Males

Bus¹,

Vasquez²,

Franke³

et al. 2012

Neuropsychobiology

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Background: Association studies of the Val66Met polymorphism and serum brain-derived neurotrophic factor (BDNF) levels have yielded conflicting results. Recently, sex-specific differences in BDNF levels were demonstrated. As these might explain the reported inconsistencies, we tested sex interactions with the Val66Met genotype on serum BDNF level. Methods: Participants (n = 548, age range 50–72 years; mean 62.8 ± 5.4 years, 267 males) were tested for rs6265 genotype and serum BDNF levels [Hardy-Weinberg equilibrium (HWE), p = 0.04]. A regression analysis with BDNF level as the dependent variable and BDNF Val66Met genotype as an independent variable was used to test the sex interaction corrected for age, smoking and depressive symptoms. Subsequently, we examined the effect of genotype on BDNF levels stratified for sex. Results: We found a significant interaction between sex and genotype on BDNF levels (p = 0.02). Male Met carriers had significantly higher BDNF levels than Val/Val homozygotes (β = 0.17, p = 0.013), while in females no effect of Val66Met genotype was found (β = –0.07, p = 0.28). Conclusion: Our findings may partly explain the inconsistent findings of earlier studies where results were influenced by male-female ratios. Replication is warranted, however, as our sample was not in HWE.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Increase in Serum Brain-Derived Neurotrophic Factor in Met Allele Carriers of the BDNF Val66Met Polymorphism Is Specific to Males

Bus¹,

Vasquez²,

Franke³

et al. 2012

Neuropsychobiology

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“…The Val to Met variant at amino acid 66 (Val66Met) results from a G758A polymorphism (rs6265) in BDNF's 11th exon. The Met allele has been associated with lower serum BDNF (Ozan et al, 2010), though this has not been consistently replicated (Duncan et al, 2009;Terracciano et al, 2010;Zhou et al, 2011). The Met allele has also been associated with increased suicide risk (Kanellopoulos et al, 2011;Pregelj et al, 2011;Sarchiapone et al, 2008), various depression-related traits (Beevers et al, 2009;Gatt et al, 2008;Gatt et al, 2010;Hayden et al, 2010;Jiang et al, 2005;Lau et al, 2010;Montag et al, 2010;Montag et al, 2008;Montag et al, 2009), and occasionally, a depression diagnosis (Aguilera et al, 2009;Borroni et al, 2009;Kim et al, 2008;Lavebratt et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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

Lotrich

Albusaysi

Ferrell

2012

Neuropsychopharmacol

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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;

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“…Besides, they observed that Brain Derived Neurotrophic Factor (BDNF) met/met and 5-HT2a receptor (5-HTR2a) 1438 A/A genotypes were associated with PSD. On the other hand, Zhou et al reported that serum BDNF concentrations were decreased in PSD patients 3 to 6 months after stroke, but this was not associated with BDNF gene Val66Met polymorphisms 41 . Tang et al suggested a possible role for genetic variation in 5-HT2c receptors (HTR2C receptors) in the pathogenesis of PSD 42 .…”

Section: Pathophysiologymentioning

confidence: 96%

Post stroke depression: clinics, etiopathogenesis and therapeutics

Pedroso¹,

Souza²,

Brunoni³

et al. 2015

Arch. Clin. Psychiatry (São Saulo)

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Background: Stroke is a major cause of morbidity and mortality worldwide. Neuropsychiatric disorders are often associated with stroke and, among them, depression is the most prevalent. Post-stroke Depression (PSD) is related to disability, failure in returning to work, impairment in interpersonal functioning and mortality. Its etiopathogenesis is still uncertain, as well as its treatment. In Brazil, there are few data on the impact of PSD. Objective: This work is dedicated to conduct a comprehensive review of the concept of PSD, its pathophysiology, morbidity and treatment. Methods: PubMed, Medline and Lilacs searches of relevant terms yielded 3,265 papers in the last 10 years. We selected original studies and reviews that addressed the aspects mentioned above. Results: We present the history of the notion of PSD and describe its epidemiology, looking to highlight Brazilian studies. Diagnostic criteria and clinical presentation were detailed, with emphasis on cognitive aspects. The four main pathophysiological theories proposed to PSD are presented and we discuss the various treatment strategies, involving psychopharmacologic options, brain stimulation techniques and psychotherapy. Discussion: This work provides comprehensive information on PSD, of great utility for clinical practice and research in this topic.

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Decreased serum brain-derived neurotrophic factor (BDNF) is associated with post-stroke depression but not withBDNFgene Val66Met polymorphism

Abstract: Serum concentrations of BDNF decrease in PSD patients and BDNF may play an important role in the pathogenesis of PSD. However, Val66Met polymorphisms are not associated with serum concentrations of BDNF. The mechanism of decreased serum BDNF requires further study.

Cited by 70 publications

References 35 publications

Increase in Serum Brain-Derived Neurotrophic Factor in Met Allele Carriers of the BDNF Val66Met Polymorphism Is Specific to Males

Increase in Serum Brain-Derived Neurotrophic Factor in Met Allele Carriers of the BDNF Val66Met Polymorphism Is Specific to Males

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

Post stroke depression: clinics, etiopathogenesis and therapeutics

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