Exploring Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Extinction Learning-Based Treatment Outcome in Obsessive-Compulsive Disorder: A Pilot Study.
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ABSTRACT:
SUBMITTER: Linkovski O
PROVIDER: S-EPMC7326118 | biostudies-literature | 2019 Jan/Feb
REPOSITORIES: biostudies-literature
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Exploring Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Extinction Learning-Based Treatment Outcome in Obsessive-Compulsive Disorder: A Pilot Study.
Linkovski Omer O Wheaton Michael G MG Zwerling Jordana J Odgerel Zagaa Z van Roessel Peter P Filippou-Frye Maria M Lombardi Anthony A Wright Brianna B Steinman Shari A SA Simpson Helen Blair HB Lee Francis F Rodriguez Carolyn I CI
Journal of clinical psychopharmacology 20190101 1
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Project description:Objective: Accumulated evidence has implicated that brain-derived neurotrophic factor (BDNF) gene polymorphisms play a role in the etiology of obsessive-compulsive disorder (OCD). A single nucleotide polymorphism in the coding exon of the BDNF gene at position 66, Val66Met (rs6265), is found to be associated with OCD in different populations, but results linking Val66Met with OCD have been inconsistent and inconclusive. In our study we performed a meta-analysis to further examine whether rs6265 genetic variants are involved in the etiology of OCD. Methods: By searching databases, relevant case-control studies were retrieved; using established inclusion criteria, we selected eligible studies for analysis. Results: Thirteen studies were identified that examined the association between the rs6265 polymorphism and OCD. After statistical analyses, no significant association was found between the rs6265 polymorphism and OCD (OR = 1.07, 95% CI = 1.00-1.15, P = 0.06 for genotype; OR = 1.06, 95% CI = 0.98-1.15, P = 0.15 for allele). However, in gender-specific analysis, female Val carriers might be a risk factor for OCD (OR = 1.36, 95% CI = 1.03-1.80, P = 0.03 for genotype; OR = 1.15, 95% CI = 1.01-1.32, P = 0.04 for allele). Conclusion: Our updated meta-analysis suggests that female carriers of the Val66Met BDNF polymorphism might be more suspectable to develop OCD.
| S-EPMC8791441 | biostudies-literature
Project description:AimBrain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family, and it promotes the development and function of dopaminergic and serotonergic neurons. The Met allele of the BDNF Val66Met polymorphism is associated with a decrease in activity-dependent secretion of BDNF compared with the Val allele, and a number of studies have provided evidence for the association between this polymorphism and obsessive-compulsive disorder (OCD). The purpose of this study was to investigate whether this functional variant of the BDNF gene is associated with OCD and treatment response in patients with OCD in the Japanese population.MethodsWe first performed a case-control association study between the BDNF Val66Met polymorphism and OCD (175 cases and 2,027 controls). Then, we examined an association between this polymorphism and treatment response in 96 patients with OCD.ResultsWe found no significant association between the Met allele and OCD risk or between the Met allele and treatment responses to selective serotonin reuptake inhibitors or serotonin reuptake inhibitor with an atypical antipsychotic (P>0.05).ConclusionOur results suggest that the BDNF Val66Met polymorphism may not be associated as a risk factor for developing OCD or with therapeutic response in patients with OCD in the Japanese population.
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Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588486 | ENA
Project description:Neurogenetics of Obsessive-Compulsive Disorder
| PRJNA588485 | ENA
Project description:Obsessive-compulsive disorder (OCD) is a highly prevalent and chronic condition that is associated with substantial global disability. OCD is the key example of the 'obsessive-compulsive and related disorders', a group of conditions which are now classified together in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and the International Classification of Diseases, 11th Revision, and which are often underdiagnosed and undertreated. In addition, OCD is an important example of a neuropsychiatric disorder in which rigorous research on phenomenology, psychobiology, pharmacotherapy and psychotherapy has contributed to better recognition, assessment and outcomes. Although OCD is a relatively homogenous disorder with similar symptom dimensions globally, individualized assessment of symptoms, the degree of insight, and the extent of comorbidity is needed. Several neurobiological mechanisms underlying OCD have been identified, including specific brain circuits that underpin OCD. In addition, laboratory models have demonstrated how cellular and molecular dysfunction underpins repetitive stereotyped behaviours, and the genetic architecture of OCD is increasingly understood. Effective treatments for OCD include serotonin reuptake inhibitors and cognitive-behavioural therapy, and neurosurgery for those with intractable symptoms. Integration of global mental health and translational neuroscience approaches could further advance knowledge on OCD and improve clinical outcomes.
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| S-EPMC4119169 | biostudies-literature
Project description:Behavioral evidence of impaired response inhibition (RI) and hyperactive error monitoring (EM) in obsessive-compulsive disorder (OCD) is inconsistent. Recent neuroimaging work suggests that EM plays a role in RI impairments in OCD, but this has rarely been investigated using behavioral measures. The aims of this study were to (1) compare RI and EM performance between adults with OCD and non-psychiatric controls (NPC) while investigating possible moderators, and (2) assess whether excessive EM influences RI in OCD. We compared RI and EM performance on the Stop-Signal Task (SST) between 92 adults with OCD and 65 NPC from two Brazilian sites. We used linear regression to investigate which variables (group, age, medication use, clinical symptomatology) influenced performance, as well as to examine possible associations between RI and EM. OCD and NPC did not differ in RI and EM. However, age moderated RI performance in OCD with a medium effect size, reflecting differential effects of age on RI between groups: age was positively associated with RI in OCD but not NPC. Further, OCD severity predicted EM with a medium to large effect size, suggesting that more symptomatic patients showed greater monitoring of their mistakes. Finally, group moderated the relationship between RI and EM with a small effect size. Our findings suggest that demographic factors may influence RI, whereas clinical factors may influence EM. Further, we found preliminary behavioral evidence to indicate that impaired RI and excessive EM are related in OCD.
| S-EPMC7313630 | biostudies-literature
Project description:ObjectiveTo examine family conflict, parental blame, and poor family cohesion as predictors of treatment outcome for youths receiving family-focused cognitive behavioral therapy (FCBT) for obsessive-compulsive disorder (OCD).MethodWe analyzed data from a sample of youths who were randomized to FCBT (n = 49; 59% male; M age = 12.43 years) as part of a larger randomized clinical trial. Youths and their families were assessed by an independent evaluator (IE) pre- and post-FCBT using a standardized battery of measures evaluating family functioning and OCD symptom severity. Family conflict and cohesion were measured via parent self-report on the Family Environment Scale (Moos & Moos, 1994), and parental blame was measured using parent self-report on the Parental Attitudes and Behaviors Scale (Peris, Benazon, et al., 2008b). Symptom severity was rated by IEs using the Children's Yale-Brown Obsessive Compulsive Scale (Scahill et al., 1997).ResultsFamilies with lower levels of parental blame and family conflict and higher levels of family cohesion at baseline were more likely to have a child who responded to FCBT treatment even after adjusting for baseline symptom severity compared with families who endorsed higher levels of dysfunction prior to treatment. In analyses using both categorical and continuous outcome measures, higher levels of family dysfunction and difficulty in more domains of family functioning were associated with lower rates of treatment response. In addition, changes in family cohesion predicted response to FCBT, controlling for baseline symptom severity.ConclusionFindings speak to the role of the family in treatment for childhood OCD and highlight potential targets for future family interventions.
| S-EPMC3378322 | biostudies-literature
Project description:In this study of the effect of bipolar status and presence of BDNF Val66Met polymorphism on differences in regional brain volumes, we hypothesized based on previous studies that 1) bipolar subjects will have smaller regional brain volumes than healthy controls; 2) BDNF Met66 allele carriers within the same population are likely to have smaller regional brain volumes as compared to Val66 homozygyotes. In our Caucasian sample of 166 bipolar subjects and 64 gender-matched healthy controls, we found significant decreases in total (p = 0.005) and regional gray matter volumes in bipolar patients compared to healthy controls, more pronounced in the inferior and posterior parts of the brain, together with a concomitant increase in total CSF (p = 0.012) particularly in the lateral ventricles (p = 0.023). However, there was no difference in white matter volumes noted by other studies. Furthermore we did not find significant differences in other brain regions that have been reported by other authors. Nor did we find a significant effect of BDNF on these measurements.
| S-EPMC3408450 | biostudies-literature
Project description:Background: Many children and adults with Obsessive-Compulsive Disorder (OCD) fail to respond to first-line pharmacological and behavioral treatments. Glutamate dysfunction may contribute to the development of OCD. N-acetylcysteine (NAC), a glutamate modulating drug, has shown to be a promising agent in adults with OCD. Methods: We conducted a double-blind, placebo-controlled clinical trial from July 2012 to January 2017. Children ages 8 to 17 years with OCD were assigned to receive NAC (up to 2700 mg/day) or the matching placebo for a period of 12 weeks. Children were required to be on stable psychiatric treatment (both medication and therapy) but were not required to be treatment-refractory. The primary outcome was OCD symptom severity as measured by the Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS). We used linear mixed models to analyze the effect of NAC compared to placebo. Results: Due to poor recruitment and eventual expiration of the study medication, enrollment was stopped at 11 children out of a planned sample size of 40. Nonetheless, NAC was associated with significant reduction in CY-BOCS total score compared to placebo (Satterthwaite's test: t (37) = 2.36, p = 0.024) with effects separating from placebo beginning at week 8. Mean CY-BOCS total score decreased in the NAC group from 21.4 ± 4.65 at baseline to 14.4 ± 5.55 at week 12. In the placebo group, mean CY-BOCS total score remained unchanged (21.3 ± 4.65). In the NAC group, 1 out of 5 participants achieved >35% improvement in CY-BOCS total score, while none of the six patients in placebo group reached this improvement level. NAC and placebo were well tolerated. One mild adverse event was reported in each group. Conclusions: Our trial suggests that there may be some initial improvement in OCD symptom severity with NAC treatment. NAC was well tolerated in the study population. Future trials should employ multiple sites and have a larger study population to further confirm any benefits of NAC.
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