Non‐replication of the brain‐derived neurotrophic factor (BDNF) association in bipolar affective disorder: A Belgian patient‐control study

Oswald, Pierre; Del-Favero, Jurgen; Massat, Isabelle; Souery, Daniel; Claes, Stephan; Broeckhoven, Christine Van; Mendlewicz, Julien

doi:10.1002/ajmg.b.30056

Cited by 64 publications

(41 citation statements)

References 11 publications

(13 reference statements)

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“…For example, some studies used broad criteria in which individuals with MDD, bipolar disorders, and dysthymia were included, 41,[44][45][46][47] whereas others included individuals with MDD only. 11,33,35,42 There are two other issues in MDD that might contribute to the inconsistency of association findings.…”

Section: Introductionmentioning

confidence: 99%

Meta-analysis of the BDNF Val66Met polymorphism in major depressive disorder: effects of gender and ethnicity

et al. 2008

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Brain-derived neurotrophic factor (BDNF) is a nerve growth factor that has antidepressant-like effects in animals and may be implicated in the etiology of mood-related phenotypes. However, genetic association studies of the BDNF Val66Met polymorphism (single nucleotide polymorphism rs6265) in major depressive disorder (MDD) have produced inconsistent results. We conducted a meta-analysis of studies comparing the frequency of the BDNF Val66Met-coding variant in depressed cases (MDD) and nondepressed controls. A total of 14 studies involving 2812 cases with DSM-III or -IV defined MDD and 10 843 nondepressed controls met the inclusion criteria. Analyses were stratified either by gender or ethnicity (Asian and Caucasian) because MDD is more prevalent in women and in Caucasians and because BDNF allele frequencies differ by ethnicity. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were provided for allelic analyses (Met versus Val), as well as for genotypic analyses (Met/Met and Val/Met versus Val/Val). In the total sample, the BDNF Val66Met polymorphism was not significantly associated with depression. However, the gender stratified analyses revealed significant effects in both the allelic and genotypic analyses in men (OR MET , 95% CI; 1.27 (1.10-1.47); OR MET/MET , 95% CI; 1.67 (1.19-2.36)). Stratification according to ethnicity did not show significant effects of the Val66Met polymorphism on MDD. Our results suggest that the BDNF Val66Met polymorphism is of greater importance in the development of MDD in men than in women. Future research into gender issues will be of interest.

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Section: Introductionmentioning

confidence: 99%

Meta-analysis of the BDNF Val66Met polymorphism in major depressive disorder: effects of gender and ethnicity

et al. 2008

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“…31 In spite of this evidence, other investigators have not been able to replicate these findings in case-control association studies. [32][33][34][35][36][37][38] In the case of MDD, some studies reported a negative association of the Val66Met BDNF polymorphism, 33,39,40 while other studies have found a haplotype containing this variant to be positively associated to the MDD phenotype. 41,42 Moreover, positive associations of this single SNP and a haplotype containing it have been reported to be associated to childhood-onset mood disorder 41,43 as well as geriatric depression.…”

Section: Introductionmentioning

confidence: 99%

A brain-derived neurotrophic factor (BDNF) haplotype is associated with antidepressant treatment outcome in mood disorders

et al. 2007

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Brain-derived neurotrophic factor (BDNF) has been studied extensively in relation to the susceptibility to mood disorders (MD), although it remains to be clarified whether BDNF is a susceptibility locus for MD phenotypes, including therapeutic response to antidepressants. We have performed a single-marker and haplotype association study of eight TagSNPs polymorphisms in the genomic region containing the BDNF gene in 342 control subjects and 374 patients with MD, and have tested the association with antidepressant treatment outcome. None of the eight single nucleotide polymorphisms (TagSNPs) was significantly associated with MD phenotype after Bonferroni correction. In the single-marker analysis, a SNP was found to be associated with the patient's state of 'remitter' after adequate trial with a single antidepressant phenotype (odds ratio (OR) ¼ 2.95; P ¼ 0.0025). We also identified a haplotype associated with this phenotype. This study supports the implication of BDNF in antidepressant treatment outcome in MD, with specific association with 5 0 upstream region of BDNF gene.

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“…These include BDNF, which showed evidence for association with bipolar disorder in two cohorts of predominantly Caucasian origin, 15,16 although this has not been replicated in several other cohorts of European and Japanese origin. [17][18][19][20] Association and functional studies have also implicated the XBP1 gene in bipolar susceptibility, 21 but again, this has not been replicated in cohorts of European and Chinese origin. 22,23 Evidence has also been reported for association of the GRIN1 gene with bipolar disorder in a cohort of predominantly European Caucasian origin.…”

Section: Introductionmentioning

confidence: 99%

Positional cloning, association analysis and expression studies provide convergent evidence that the cadherin gene FAT contains a bipolar disorder susceptibility allele

et al. 2006

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A susceptibility locus for bipolar disorder was previously localized to chromosome 4q35 by genetic linkage analysis. We have applied a positional cloning strategy, combined with association analysis and provide evidence that a cadherin gene, FAT, confers susceptibility to bipolar disorder in four independent cohorts (allelic P-values range from 0.003 to 0.024). In two case-control cohorts, association was identified among bipolar cases with a family history of psychiatric illness, whereas in two cohorts of parent-proband trios, association was identified among bipolar cases who had exhibited psychosis. Pooled analysis of the case-control cohort data further supported association (P = 0.0002, summary odds ratio = 2.31, 95% CI: 1.49-3.59). We localized the bipolar-associated region of the FAT gene to an interval that encodes an intracellular EVH1 domain, a domain that interacts with Ena/VASP proteins, as well as putative b-catenin binding sites. Expression of Fat, Catnb (b-catenin), and the three genes (Enah, Evl and Vasp) encoding the Ena/VASP proteins, were investigated in mice following administration of the mood-stabilizing drugs, lithium and valproate. Fat was shown to be significantly downregulated (P = 0.027), and Catnb and Enah were significantly upregulated (P = 0.0003 and 0.005, respectively), in response to therapeutic doses of lithium. Using a protein interaction map, the expression of genes encoding murine homologs of the FAT (ft)-interacting proteins was investigated. Of 14 interacting molecules that showed expression following microarray analysis (including several members of the Wnt signaling pathway), eight showed significantly altered expression in response to therapeutic doses of lithium (binomial P = 0.004). Together, these data provide convergent evidence that FAT and its protein partners may be components of a molecular pathway involved in susceptibility to bipolar disorder.

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Non‐replication of the brain‐derived neurotrophic factor (BDNF) association in bipolar affective disorder: A Belgian patient‐control study

Cited by 64 publications

References 11 publications

Meta-analysis of the BDNF Val66Met polymorphism in major depressive disorder: effects of gender and ethnicity

Meta-analysis of the BDNF Val66Met polymorphism in major depressive disorder: effects of gender and ethnicity

A brain-derived neurotrophic factor (BDNF) haplotype is associated with antidepressant treatment outcome in mood disorders

Positional cloning, association analysis and expression studies provide convergent evidence that the cadherin gene FAT contains a bipolar disorder susceptibility allele

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