scholarly journals Brain derived neurotrophic factor (BDNF) Val66Met polymorphism is not risk factor for bipolar disorder

2019 ◽  
Author(s):  
Vandana Rai ◽  
Farhin Jamal ◽  
Pradeep Kumar

AbstractBipolar disorder (BPD) is a psychiatric disease, characterized by the cycles of mania and depression. Several genetic studies investigated BDNF gene Val66Met polymorphism as risk factor for BPD, but results were inconclusive. Therefore, present meta-analysis was performed to reevaluate the BDNF Val66Met polymorphism and BPD association. Four databases (Pubmed, Springer Link, Science Direct and Google Scholar) were searched for eligible studies up to March 31,2018. Pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated to estimate the strength of the association. All statistical analyses were done by MetaAnalyst and Mix program. Forty studies with a total of 28,787 subjects (10,085 cases and 18,702 controls) were included in this meta-analysis. Overall, pooled analysis indicated that there was no significant association between BDNF Val66Met polymorphism and BPD risk under all five genetic models (ORA vs.G =0.99, 95%CI= 0.94-1.03, p=0.49; ORAG vs. GG= 0.1.02, 95%CI= 0.95-1.07, p= 0.57; ORAA vs. GG = 0.98, 95%CI=0.89-1.08, p=0.75; ORAA+AG vs. GG= 1.0, 95%CI= 0.94-1.06, p= 0.89;ORAA vs. AG+GG= 0.96, 95%CI= 0.89-1.05, p= 0.47). Similarly, no significant association was observed in ethnicity based subgroup analysis in both Asian and Caucasian population. However, significant association was found in subtype analysis between BDNF Val66Met and BPDII (ORAA+AG vs. GG= 1.21, 95%CI= 1.06-1.37, p= 0.003) but not with BPDI. These findings suggested that the BDNF Val66Met polymorphism confer no genetic susceptibility to BPD I but risk for BPDII.

2021 ◽  
Vol 61 (1) ◽  
Author(s):  
Angela Shiratsu Yamada ◽  
Flavia Tasmim Techera Antunes ◽  
Camila Ferraz ◽  
Alessandra Hubner de Souza ◽  
Daniel Simon

Abstract Background The Val66Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene is a potential biomarker of vulnerability to pain. Thus, the present study aimed to investigate the association of this polymorphism with clinical and biopsychosocial factors in patients with chronic low back pain (CLBP). Methods A total of 107 individuals with CLBP answered questionnaires that were validated and adapted for the Brazilian population, including the Brief Inventory of Pain, the Central Sensitization Inventory, the Roland Morris Disability Questionnaire, the Tampa Scale for Kinesiophobia, the Pain Catastrophizing Scale, the Survey of Pain Attitude-Brief, and the Hospital Anxiety and Depression Scale. All of the subjects were genotyped for the BDNF Val66Met polymorphism. Results The sample showed moderate scores of disability, central sensitization, and kinesiophobia, in addition to mild anxiety, hopelessness, and ruminant thoughts. No significant association was observed between the Val66Met polymorphism and the variables analyzed. Besides, there was no relationship between the BDNF Val66Met polymorphism with CSI, catastrophization, or disabilities that were generated by CLBP. Conclusion The results showed that the Val66Met polymorphism of the BDNF gene was not associated with clinical and biopsychosocial characteristics of CLBP in the sample studied.


2020 ◽  
Vol 11 ◽  
Author(s):  
Li He ◽  
Yanhui Liao ◽  
Qiuxia Wu ◽  
Tieqiao Liu

Background: Several studies had examined the association between brain-derived neurotrophic factor (BDNF) Val66Met polymorphism and methamphetamine (METH) use disorder, whereas the results were conflicting. The aim of this study was to conduct a meta-analysis to achieve a pooled effect size of the association between BDNF Val66Met polymorphism and METH use disorder.Methods: Literature searches were conducted in PubMed, EMBASE, and Cochrane Library up to July, 2020. All relevant studies on the relationship of BDNF Val66Met polymorphism and METH addiction were retrieved. Pooled odds ratios (ORs) with 95% confidence intervals (95% CIs) were calculated in the dominant, recessive, co-dominant, and allele model to appraise the association.Results: Seven case–control studies with a total of 2,204 subjects (956 METH-dependent cases and 1,248 healthy controls) were included in this meta-analysis. The results showed a significant correlation between BDNF Val66Met polymorphism and METH dependence in overall population under different genetic models. However, subgroup analysis indicated that the association only existed in Han Chinese but not in other Asian populations.Conclusion: Although the current data indicate that BDNF Val66Met polymorphism might be a potential genetic factor for METH use disorder, more researches are needed to prove its role in different populations.


CNS Spectrums ◽  
2012 ◽  
Vol 17 (3) ◽  
pp. 155-163 ◽  
Author(s):  
Asuka Katsuki ◽  
Reiji Yoshimura ◽  
Taro Kishi ◽  
Hikaru Hori ◽  
Wakako Umene-Nakano ◽  
...  

ObjectWe investigated an association between the polymorphism of brain-derived neurotrophic factor (BDNF) gene Val66Met and the response to mirtazapine in Japanese patients with major depressive disorder (MDD). We also examined mirtazapine's effects on the serum BDNF and plasma levels of catecholamine metabolites in these patients.MethodsEighty-four patients who met the DSM-IV-TR criteria for MDD were treated with only mirtazapine for 4 weeks. The BDNF Val66Met polymorphism was detected by direct sequencing in the region, and serum BDNF levels and plasma levels of catecholamine metabolites were measured by ELISA and HPLC-ECD, respectively.ResultsMirtazapine treatment for 4 weeks significantly increased serum BDNF levels in the responders, whereas nonresponders showed significant decreases. No association was found between either of the two genotypes (Val/Val vs. Met-carriers) and the response to mirtazapine at T4 or the serum BDNF levels at T0. Mirtazapine did not alter the plasma levels of homovanillic acid (HVA) or 3-methoxy-4-hydroxyphenylglycol (MHPG).DiscussionThe dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNF Val66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels.ConclusionSerum BDNF levels, but not plasma levels of HVA or MHPG, and BDNF Val66Met polymorphism are related to the mirtazapine response in MDD.


2009 ◽  
Vol 39 (11) ◽  
pp. 1831-1839 ◽  
Author(s):  
C. Montag ◽  
B. Weber ◽  
K. Fliessbach ◽  
C. Elger ◽  
M. Reuter

BackgroundThe role of the brain-derived neurotrophic factor (BDNF) in the pathogenesis of affective disorders such as depression has been controversial. Mounting evidence comes from structural imaging, that the functional BDNF Val66Met polymorphism influences the hippocampal volume with carriers of the 66Met allele (Val/Met and Met/Met group) having smaller hippocampi. Given that stress-induced atrophy of the hippocampus is associated with the pathogenesis of affective disorders, the functional BDNF Val66Met polymorphism could be an incremental risk factor.MethodEighty-seven healthy Caucasian participants underwent structural imaging and were genotyped for the BDNF Val66Met polymorphism. Data were analysed by means of voxel-based morphometry (VBM).ResultsRegion of interest (ROI) analyses revealed an association between the 66Met allele and smaller parahippocampal volumes and a smaller right amygdala. In addition, the whole-brain analysis showed that the thalamus, fusiformus gyrus and several parts of the frontal gyrus were smaller in 66Met allele carriers.ConclusionsThis study demonstrates that the impact of the BDNF Val66Met polymorphism is not confined to the hippocampus but also extends to the parahippocampal gyrus and the amygdala.


2014 ◽  
Vol 152 (2-3) ◽  
pp. 365-372 ◽  
Author(s):  
Itaru Miura ◽  
Jian-Ping Zhang ◽  
Masahiro Nitta ◽  
Todd Lencz ◽  
John M. Kane ◽  
...  

2012 ◽  
Vol 36 (9) ◽  
pp. 2165-2177 ◽  
Author(s):  
Joseph P. Kambeitz ◽  
Sagnik Bhattacharyya ◽  
Lana M. Kambeitz-Ilankovic ◽  
Isabel Valli ◽  
David A. Collier ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document