Regression analysis determined the extent to which psychiatric comorbidity, illness severity, OCD symptom dimensions, childhood trauma history, and the Val66Met (rs6265) polymorphism of the brainderived neurotrophic factor (BDNF) gene predict lifetime suicidal ideation and attempts in adults with OCD.
We can conclude that transcriptional regulation of BDNF in OCD engages epigenetic mechanisms, and can suggest that this is likely evoked by the long-term pharmacotherapy.
In this study, we perform a case control analysis of association of a single nucleotide polymorphism rs6265(Val66Met) in Brain Derived Neurotrophic Factor gene, that has been previously implicated in a variety of psychiatric syndromes, and examine its association with symptom dimensions of OCD.
Brain-derived neurotrophic factor (BDNF) is an interesting candidate for molecular analysis in OCD on the basis of potential functional relevance, positive association studies, and reported interaction between this gene and other neurotransmitters implicated in this disorder.
Our study supports the involvement of the BDNFVal66Met polymorphism as a common genetic susceptibility for OCD and TS in the Chinese Han population, showing specific gender trends.
The purpose of this study was to derive a more precise estimation of the association between BDNFVal66Met polymorphism and OCD susceptibility by a meta-analysis.
Although no significant association was observed between BDNFVal66Met and the development of OCD, interaction analysis indicated that the BDNF Met-allele interacted with childhood emotional abuse to increase the risk of OCD significantly in a dose-dependent manner (p = 0.024).
BDNF promote the function and growth of 5-HT neurons in the brain and modulate the synaptic plasticity of DRD3-secreting neurons in the striatum, suggesting involvement of BDNF in the mediation of obsessive-compulsive disorder.
In this article, we briefly review previous work regarding clinical and demographical factors associated with drug response in OCD, then focus on recent findings regarding candidate genes which may influence drug response, including those in the serotonin system, brain-derived neurotrophic factor and the glutamate transporter gene.
Genetic variation in BDNF may be associated with treatment response in exposure-based CBT in OCD, especially in those patients exhibiting contamination/cleaning symptoms.
Haplotype analysis revealed a significant association between OCD and a five-marker protective haplotype located toward the 5' of the BDNF gene (odds ratio [OR] = .80; 95% confidence interval [CI] = .69-.92; permutation p value = .006) containing the functional valine (Val)66-to-methionine (Met) variant.
As several other uncommon, less well quantitated genetic variations occur with an OCD phenotype, including chromosomal anomalies and some other rare gene variants (SGCE, GCH1 and SLITRK1), a tentative conclusion is that OCD resembles other complex disorders in being etiologically heterogeneous and in having both highly penetrant familial subtypes associated with rare alleles or chromosomal anomalies, as well as having a more common, polygenetic form that may involve polymorphisms in such genes as BDNF, COMT, GRIN2beta, TPH2, HTR2A and SLC1A1.
The aim of the present study was to investigate the role that the val66met variant within the gene encoding brain-derived neurotrophic factor (BDNF) may play in mediating the development of selected OCD subtypes accounting for the aforementioned confounding factors.