Investigating the role of the brain-derived neurotrophic factor (BDNF)<i>val66met</i>variant in obsessive-compulsive disorder (OCD)

Hemmings, Sı̂an M.J.; Kinnear, Craig; Merwe, Lize van der; Löchner, Christine; Corfield, Valerie A.; Moolman‐Smook, Johanna C.; Stein, Dan J.

doi:10.1080/15622970701245003

Cited by 67 publications

(70 citation statements)

References 38 publications

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“…Previous studies have implicated both the BDNF Val- (Hall et al, 2003) and Met-alleles in the development of OCD (Hemmings et al, 2008;Katerberg et al, 2009). Our group has previously found that the Met-allele represented a risk allele for the development of OCD in males, while females homozygous for the Val-allele exhibited more severe OCD symptoms (Hemmings et al, 2008;Katerberg et al, 2009).…”

Section: Discussionmentioning

confidence: 62%

“…Hall et al (2003) observed an association between the Val-allele and childhood-onset OCD, although this result was not replicated in a later study (Mossner et al, 2005). Our group observed an association between the Met-allele and OCD in male patients with early-onset OCD (Hemmings et al, 2008). However, in the same study, the Val/Val genotype was found to be associated with increased severity of OCD in females.…”

Section: Introductionmentioning

confidence: 54%

“…The BDNF Val66Met polymorphism (rs6265) was genotyped as previously described (Hemmings et al, 2008).…”

Section: Dna Extraction Amplification and Genotypingmentioning

confidence: 99%

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BDNF Val66Met modifies the risk of childhood trauma on obsessive-compulsive disorder

Hemmings

Löchner

Merwe

et al. 2013

Journal of Psychiatric Research

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Abstract:Childhood trauma has been linked to the development of later psychopathology, including obsessive-compulsive disorder (OCD). Although evidence exists to suggest that genetic and environmental factors are involved in the aetiology of OCD, little attention has been paid to the interactions that exist between genes and environment. The aim of this study was to investigate gene-byenvironment interactions between childhood trauma and the BDNF Val66Met variant in patients with OCD.Childhood trauma was assessed in 134 OCD patients and 188 controls using the Childhood Trauma Questionnaire (CTQ). Linear regression models were used for statistical analyses. Geneeenvironment interactions were estimated by including a combined genotype and CTQ score in the models as interaction terms. All analyses were adjusted for age, gender, CTQ minimisation-denial score and home language by including them in the logistic regression models as covariates.Childhood trauma, specifically emotional abuse and neglect, increased the odds of having OCD significantly (p < 0.001). Although no significant association was observed between BDNF Val66Met and the development of OCD, interaction analysis indicated that the BDNF Met-allele interacted with childhood emotional abuse to increase the risk of OCD significantly in a dose-dependent manner (p < 0.024). To our knowledge, this is one of the first studies to investigate geneeenvironment interactions in OCD, and the findings indicate the importance of collating genetic and environmental variables in future studies.

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Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 54%

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BDNF Val66Met modifies the risk of childhood trauma on obsessive-compulsive disorder

Hemmings

Löchner

Merwe

et al. 2013

Journal of Psychiatric Research

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“…The BDNF Val66Met polymorphism (rs6265) was genotyped as previously described (Hemmings et al, 2008). …”

Section: Methodsmentioning

confidence: 99%

“…Compared with the Val66 allele, the Met66 allele is associated with a decrease in activity-dependent secretion of BDNF (Egan et al, 2003). BDNF has received attention due to its evident role in anxiety and mood disorders (Angelucci et al, 2014; Hemmings et al, 2008; Li, Chang, & Xiao, 2016; Martinowich et al, 2007; Molendijk et al, 2014; Suliman, Hemmings, & Seedat, 2013), although findings have been inconsistent across studies (Frustaci, Pozzi, Gianfagna, Manzoli, & Boccia, 2008; Hong, Liou, & Tsai, 2012; Lam, Cheng, Hong, & Tsai, 2004; Minelli et al, 2011; Notaras et al, 2015; Surtees et al, 2007; Wang et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

Martin

Hemmings

Kidd

et al. 2018

European Journal of Psychotraumatology

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Background: Anxiety disorders in youth are attributable to multiple causal mechanisms, comprising biological vulnerabilities, such as genetics and temperament, and unfavourable environmental influences, such as childhood maltreatment (CM).Objective: A gene-environment (G x E) interaction study was conducted to determine the interactive effect of the BDNF Val66Met polymorphism and CM to increase susceptibility to anxiety sensitivity (AS) in a sample of mixed race adolescents.Method: Participants (n = 308, mean age = 15.8 years) who were all secondary school students and who completed measures for AS and CM were genotyped for the BDNF Val66Met polymorphism. Hierarchical multiple regression analysis was conducted to assess G x E influences on AS. Age and gender were included in the models as covariates as age was significantly associated with AS total score (p < .05), and females had significantly higher AS scores than males (p < .05).Results: A main effect of CM on AS was evident (p < .05), however, no main effect of BDNF genotype on AS was observed (p > .05). A non-significant G x E effect on AS was revealed (p < .05).Conclusions: Our results suggest that CM does not have a moderating role in the relationship between the BDNF Val66Met genotype and the increased risk of anxiety-related phenotypes, such as AS. Given the exploratory nature of this study, findings require replication in larger samples and adjustment for population stratification to further explore the role of BDNF Val66Met and CM on AS in mixed race adolescents.

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The role of the brain‐derived neurotrophic factor (BDNF) val66met variant in the phenotypic expression of obsessive‐compulsive disorder (OCD)

Katerberg

Löchner

Cath

et al. 2009

American J of Med Genetics Pt B

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Evidence suggests that the Val66Met variant of the brain-derived neurotrophic factor (BDNF) gene may play a role in the etiology of Obsessive-Compulsive Disorder (OCD). In this study, the role of the BDNF Val66Met variant in the etiology and the phenotypic expression of OCD is investigated. Associations between the BDNF Val66Met variant and OCD, obsessive-compulsive symptom dimensions, Yale-Brown Obsessive Compulsive Scale (YBOCS) severity scores, age of onset and family history of obsessive-compulsive symptoms were assessed. The BDNF Val66Met variant was genotyped in 419 patients with sub-/clinical OCD and 650 controls. No differences in allele or genotype frequency were observed between cases and controls. In females with OCD, the Met66Met genotype was associated with later age of onset and a trend for a negative family history, whereas the Val66Val genotype was associated with a trend for lower YBOCS severity scores. Item-level factor analysis revealed six factors: 1) Contamination/cleaning; 2) Aggressive obsessions/checking; 3) Symmetry obsessions, counting, ordering and repeating; 4) Sexual/religious obsessions; 5) Hoarding and 6) Somatic obsessions/checking. A trend was found for a positive association between Factor 4 (Sexual/religious obsessions) and the BDNF Val66Val genotype. The results suggest that BDNF function may be implicated in the mediation of OCD. We found that for the BDNF Met66Met genotype may be associated with a milder phenotype in females and a possible role for the BDNF Val66Val genotype and the BDNF Val66 allele in the sexual/religious obsessions.

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Investigating the role of the brain-derived neurotrophic factor (BDNF)val66metvariant in obsessive-compulsive disorder (OCD)

Cited by 67 publications

References 38 publications

BDNF Val66Met modifies the risk of childhood trauma on obsessive-compulsive disorder

BDNF Val66Met modifies the risk of childhood trauma on obsessive-compulsive disorder

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

The role of the brain‐derived neurotrophic factor (BDNF) val66met variant in the phenotypic expression of obsessive‐compulsive disorder (OCD)

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