The BDNF Val66Met polymorphism impacts parahippocampal and amygdala volume in healthy humans: incremental support for a genetic risk factor for depression

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 153 ◽  
pp. S189
Author(s):  
Silvia Alemany ◽  
Aldo Córdova-Palomera ◽  
Carles Falcón ◽  
Mar Fatjó-Vilas ◽  
Ximena Goldberg ◽  
...  

2012 ◽  
Vol 2 (6) ◽  
pp. 726-731 ◽  
Author(s):  
Ruud Smolders ◽  
Mark Rijpkema ◽  
Barbara Franke ◽  
Guillén Fernández

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.


2019 ◽  
Vol 243 ◽  
pp. 552-558 ◽  
Author(s):  
G.M. Mandolini ◽  
M. Lazzaretti ◽  
A. Pigoni ◽  
G. Delvecchio ◽  
J.C. Soares ◽  
...  

2015 ◽  
Vol 15 (3) ◽  
pp. 625-643 ◽  
Author(s):  
Ana Kim ◽  
◽  
Anne M. Fagan ◽  
Alison M. Goate ◽  
Tammie L. S. Benzinger ◽  
...  

Author(s):  
Laila Cigana Schenkel ◽  
Jair Segal ◽  
Juliana Allebrand Becker ◽  
Gisele Gus Manfro ◽  
Marino Muxfeldt Bianchin ◽  
...  

Author(s):  
Raffaele Dubbioso ◽  
Giovanni Pellegrino ◽  
Federico Ranieri ◽  
Giovanni Di Pino ◽  
Fioravante Capone ◽  
...  

Preclinical studies have demonstrated that Brain-Derived Neurotrophic Factor (BDNF) plays a crucial role in the homeostatic regulation of cortical excitability and excitation/inhibition balance. Using transcranial magnetic stimulation (TMS) techniques we investigated whether BDNF polymorphism could influence cortical excitability of the left and right primary motor cortex in healthy humans. Twenty-nine participants were recruited and genotyped for the presence of the BDNF Val66Met polymorphism, namely homozygous for the valine allele (Val/Val), heterozygotes (Val/Met), and homozygous for the methionine allele (Met/Met). Blinded to the latter, we evaluated inhibitory and facilitatory circuits of the left (LH) and right motor cortex (RH) by measuring resting (RMT) and active motor threshold (AMT), short interval intracortical inhibition (SICI) and intracortical facilitation (ICF). For each neurophysiological metric we also considered the inter-hemispheric balance expressed by the Laterality Index (LI). Val/Val participants (n= 21) exhibited an overall higher excitability of the LH compared to the RH, as probed by lower motor thresholds, lower SICI and higher ICF. Val/Val participants displayed positive LI, especially for AMT and ICF (all p< 0.05), indicating higher LH excitability and more pronounced inter-hemispheric excitability imbalance as compared to Met carriers. Our preliminary results suggest that BDNF Val66Met polymorphism might influence interhemispheric balance of motor cortex excitability.


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