Brain-derived neurotrophic factor gene polymorphism (Val66Met) and citalopram response in major depressive disorder

Choi, Moon-Gi; Kang, Rhee Hun; Lim, Seung-Taik; Oh, Kap Sung; Lee, Min-Soo

doi:10.1016/j.brainres.2006.08.012

Cited by 168 publications

(125 citation statements)

References 47 publications

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“…The methods used for genotyping in the different reports included restriction fragment length polymorphism analysis, 19 38 and an Illumina Beadarray-based analysis. 39 …”

Section: Inclusion Criteriamentioning

confidence: 99%

“…11,19,21,33,34,36,37,40,42,43 Statistical analysis The meta-analysis examined the allelic association of the Met allele with the risk of MDD relative to the Val allele (OR Met versus Val). Besides this, genotypic ORs were calculated for the heterozygous Val/Met and homozygous Met/Met genotypes separately, with the Val/Val genotype as the reference.…”

Section: Data Extractionmentioning

confidence: 99%

“…In Caucasian populations, the frequency of the Met allele is 25-32%, 17,18 whereas in Asian populations the Met allele is more frequent, around 40-50%. [19][20][21] Currently, it is still unclear what the consequences of the Val66Met polymorphism are on brain function, as both alleles have been associated with different disease processes including substance-related disorders, schizophrenia, and eating disorders. 22 The risk allele for depression and depression-related traits has also not been clearly defined.…”

Section: Introductionmentioning

confidence: 99%

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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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“…The methods used for genotyping in the different reports included restriction fragment length polymorphism analysis, 19 38 and an Illumina Beadarray-based analysis. 39 …”

Section: Inclusion Criteriamentioning

confidence: 99%

Section: Data Extractionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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

et al. 2008

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“…93 In contrast, three recent studies from Chinese and Korean populations have reported no association between this BDNF polymorphism and depression. [94][95][96] While such negative results could be due to underpowered sample sizes and differences in subject ethnicity, 93 recent studies carried out using much larger samples, using tens of thousands of subjects, have failed to confirm the association. 97,98 It should be noted however, that even for the most widely studied genetic variants associated with depression and anxiety, such as the serotonin transporter, meta-analyses have reported inconclusive findings, identifying a significant lack of inconsistency across studies.…”

Section: Evidence Formentioning

confidence: 99%

Is it time to reassess the BDNF hypothesis of depression?

2007

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The brain-derived neurotrophic factor (BDNF) hypothesis of depression postulates that a loss of BDNF is directly involved in the pathophysiology of depression, and that its restoration may underlie the therapeutic efficacy of antidepressant treatment. While this theory has received considerable experimental support, an increasing number of studies have generated evidence which is not only inconsistent, but also directly contradicts the hypothesis. This article provides a critical review of the clinical and preclinical studies which have been responsible for this controversy, outlining pharmacological, behavioural and genetic evidence which demonstrates the contrasting role of BDNF in regulating mood and antidepressant effects throughout the brain. I will also review key studies, both human and animal, which have investigated the association of a BDNF single-nucleotide polymorphism (Val66Met) with depression pathogenesis, and detail the number of inconsistencies which also afflict this novel area of BDNF research. The article will conclude by discussing why now is a critical time to reassess the original BDNF hypothesis of depression, and look towards the formation of new models that can provide a more valid account of the complex relationships between growth factors, mood disorders and their treatment.

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“…Polymorphisms in the BDNF gene have also been linked to antidepressant efficacy. Patients with the Met66Met genotype have a better response to fluvoxamine, milnacipran and citalopram (Choi et al, 2006;Yoshida et al, 2006). However, therapeutics that globally target TrkB may not be universally efficacious in depression or anxiety where individual variation and regional differences exist in the effect of BDNF.…”

Section: Bdnf As a Therapeutic Target For Alcoholism?mentioning

confidence: 99%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

125

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Brain Derived Neurotrophic Factor (BDNF) has emerged as a regulator of development, plasticity and, recently, addiction. Decreased neurotrophic activity may be involved in ethanol-induced neurodegeneration in the adult brain and in the etiology of alcohol-related neurodevelopmental disorders. This can occur through decreased expression of BDNF or through inability of the receptor to transduce signals in the presence of ethanol. In contrast, recent studies implicate region-specific up-regulation of BDNF and associated signaling pathways in anxiety, addiction and homeostasis after ethanol exposure. Anxiety and depression are precipitating factors for substance abuse and these disorders also involve region-specific changes in BDNF in both pathogenesis and response to pharmacotherapy. Polymorphisms in the genes coding for BDNF and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of alcoholism. This review summarizes historical and pre-clinical data on BDNF and TrkB as it relates to ethanol toxicity and addiction. Many unresolved questions about region-specific changes in BDNF expression and the precise role of BDNF in neuropsychiatric disorders and addiction remain to be elucidated. Resolution of these questions will require significant integration of the literature on addiction and comorbid psychiatric disorders that contribute to the development of alcoholism.

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Brain-derived neurotrophic factor gene polymorphism (Val66Met) and citalopram response in major depressive disorder

Cited by 168 publications

References 47 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

Is it time to reassess the BDNF hypothesis of depression?

Ethanol–BDNF interactions: Still more questions than answers

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