The Val66Met Polymorphism at the BDNF Gene does not Influence Wisconsin Card Sorting Test Results in Children and Adolescents with Bipolar Disorder

Zeni, Cristian Patrick; Tramontina, Silzá; Zeni, Thamis; Coelho, Roberta Paula Schell; Pheula, Gabriel Ferreira; Bernardi, Julio M.; Maldaner, Ursula; Silva, Talita Lopes; Salatino-Oliveira, Angélica; Hutz, Mara H.; Rohde, Luis Augusto

doi:10.1016/j.rbp.2012.02.007

Cited by 10 publications

(11 citation statements)

References 34 publications

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“…The following genotype frequencies were evident in our mixed race sample: Val66Val (75.65%, 233/308), Val66Met (22.08%, 68/308) and Met66Met (2.3%, 7/308). These frequencies are generally in line with those determined in Caucasian samples (Carver et al, 2011; Gatt et al, 2009; Pivac et al, 2009; Surtees et al, 2007; Zeni et al, 2013) and in South African mixed race samples (Dalvie et al, 2014), and confirm the low rates of Met66 allele carriers evident in ethnic groups in sub-Saharan Africa (Petryshen et al, 2009). Given the low frequency of Met66Met genotype carriers, Val66Met and Met66Met genotypes were combined (24.35%, 75/308) for genotypic analyses to increase statistical power.…”

Section: Resultssupporting

confidence: 83%

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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Section: Resultssupporting

confidence: 83%

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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“…However, no other study has done a longitudinal investigation of the correlation between changes of plasma BDNF and changes of cognitive function in the subtypes of BD while considering the effects of the BDNF Val66Met polymorphism. Inconsistent results were found regarding the association between the BDNF Val66Met polymorphism and cognitive function in BD; one suggested a non-significant association 56 , one said that those with Val/Val genotypes performed better 31 , two said that those with the Met allele performed worse 57,58 , and two attribute the worse performance of BD patients with the Met allele to the smaller hippocampus volumes of patients with the Val/Val genotype 32,58 . Some researchers have reported a non-significant correlation between peripheral BDNF levels and WCST scores 59 and executive function in BP-I 60,61 .…”

Section: Discussionmentioning

confidence: 99%

The Correlation between Plasma Brain-derived Neurotrophic Factor and Cognitive Function in Bipolar Disorder is Modulated by the BDNF Val66Met Polymorphism

Lee

2017

Eur. psychiatr.

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We explored the effect of the Brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) on correlation between changes in plasma BDNF levels with cognitive function and quality of life (QoL) after 12 weeks of treatment in bipolar disorder (BD). Symptom severity and plasma BDNF levels were assessed upon recruitment and during weeks 1, 2, 4, 8 and 12. QoL, the Wisconsin Card Sorting Test (WCST), and the Conners' Continuous Performance Test (CPT) were assessed at baseline and endpoint. The BDNF Val66Met polymorphism was genotyped. Changes in cognitive function and QoL over 12 weeks were reduced using factor analysis for the evaluation of their correlations with changes in plasma BDNF. Five hundred forty-one BD patients were recruited and 65.6% of them completed the 12-week follow-up. Changes in plasma BDNF levels with factor 1 (WCST) were significantly negatively correlated (r = −0.25, p = 0.00037). After stratification of BD subtypes and BDNF genotypes, this correlation was significant only in BP-I and the Val/Met genotype (r = −0.54, p = 0.008). We concluded that changes in plasma BDNF levels significantly correlated with changes in WCST scores in BD and is moderated by the BDNF Val66Met polymorphism and the subtype of BD.Bipolar disorder (BD) is characterized by recurrent episodes of dysregulated moods 1,2 . With high heritability 3 , genetic factors had been regarded as an important etiology for BD. The most frequently seen subtypes of BD are bipolar I disorder (BP-I) and bipolar II disorder (BP-II). Being a chronic mental disorder, BD is increasingly regarded as a neurodegenerative disorder supported by imaging studies 4,5 . Brain-derived neurotrophic factor (BDNF) is an important protein for neuron development, growth and survival 6 . BDNF is robustly expressed

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“…28,29 Although international differences in BD are less well studied in youth as compared to adults, there now are PBD data from multiple countries including Australia/New Zealand, Brazil, China, France, India, Italy, South Korea, Spain, the Netherlands, Turkey, and the UK. 30 In addition to the epidemiologic studies reviewed above, international BD data now include phenomenological, 19,31–33 comorbidity, 19,34 longitudinal, 35,36 treatment, 37,38 neuroimaging and biomarker, 39–41 and high-risk studies. 42,43 Numerous commentaries discuss purported international differences in the prevalence of PBD, which may be attributable to including more subtypes, 1 differences in the interview method, 44 training, 23,45 or the type of sample studied (predominantly manic, depressive, treatment-seeking or registry), or a combination of these.…”

Section: | International Findingsmentioning

confidence: 99%

The International Society for Bipolar Disorders Task Force report on pediatric bipolar disorder: Knowledge to date and directions for future research

et al. 2017

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Objectives Over the past two decades, there has been tremendous growth in research regarding bipolar disorder (BD) among children and adolescents (ie, pediatric BD [PBD]). The primary purpose of this article is to distill the extant literature, dispel myths or exaggerated assertions in the field, and disseminate clinically relevant findings. Methods An international group of experts completed a selective review of the literature, emphasizing areas of consensus, identifying limitations and gaps in the literature, and highlighting future directions to mitigate these gaps. Results Substantial, and increasingly international, research has accumulated regarding the phenomenology, differential diagnosis, course, treatment, and neurobiology of PBD. Prior division around the role of irritability and of screening tools in diagnosis has largely abated. Gold-standard pharmacologic trials inform treatment of manic/mixed episodes, whereas fewer data address bipolar depression and maintenance/continuation treatment. Adjunctive psychosocial treatment provides a forum for psychoeducation and targets primarily depressive symptoms. Numerous neurocognitive and neuroimaging studies, and increasing peripheral biomarker studies, largely converge with prior findings from adults with BD. Conclusions As data have accumulated and controversy has dissipated, the field has moved past existential questions about PBD toward defining and pursuing pressing clinical and scientific priorities that remain. The overall body of evidence supports the position that perceptions about marked international (US vs elsewhere) and developmental (pediatric vs adult) differences have been overstated, although additional research on these topics is warranted. Traction toward improved outcomes will be supported by continued emphasis on pathophysiology and novel therapeutics.

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The Val66Met Polymorphism at the BDNF Gene does not Influence Wisconsin Card Sorting Test Results in Children and Adolescents with Bipolar Disorder

Abstract: Our findings from this sample of children and adolescents with BD do not replicate results from studies of adults and suggest the existence of differences in the neurobiology of this disorder across the life cycle. Investigations of larger samples are necessary to confirm these data.

Cited by 10 publications

References 34 publications

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

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

The Correlation between Plasma Brain-derived Neurotrophic Factor and Cognitive Function in Bipolar Disorder is Modulated by the BDNF Val66Met Polymorphism

The International Society for Bipolar Disorders Task Force report on pediatric bipolar disorder: Knowledge to date and directions for future research

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