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No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population
AIM: Brain-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...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Dove Medical Press
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4795591/ https://www.ncbi.nlm.nih.gov/pubmed/27042072 http://dx.doi.org/10.2147/NDT.S102100 |
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author | Umehara, Hidehiro Numata, Shusuke Kinoshita, Makoto Watanabe, Shinya Nakaaki, Shutaro Sumitani, Satsuki Ohmori, Tetsuro |
author_facet | Umehara, Hidehiro Numata, Shusuke Kinoshita, Makoto Watanabe, Shinya Nakaaki, Shutaro Sumitani, Satsuki Ohmori, Tetsuro |
author_sort | Umehara, Hidehiro |
collection | PubMed |
description | AIM: Brain-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. METHODS: We 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. RESULTS: We 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). CONCLUSION: Our 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. |
format | Online Article Text |
id | pubmed-4795591 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-47955912016-04-01 No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population Umehara, Hidehiro Numata, Shusuke Kinoshita, Makoto Watanabe, Shinya Nakaaki, Shutaro Sumitani, Satsuki Ohmori, Tetsuro Neuropsychiatr Dis Treat Original Research AIM: Brain-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. METHODS: We 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. RESULTS: We 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). CONCLUSION: Our 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. Dove Medical Press 2016-03-11 /pmc/articles/PMC4795591/ /pubmed/27042072 http://dx.doi.org/10.2147/NDT.S102100 Text en © 2016 Umehara et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Umehara, Hidehiro Numata, Shusuke Kinoshita, Makoto Watanabe, Shinya Nakaaki, Shutaro Sumitani, Satsuki Ohmori, Tetsuro No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title | No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title_full | No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title_fullStr | No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title_full_unstemmed | No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title_short | No association between BDNF Val66Met polymorphism and treatment response in obsessive-compulsive disorder in the Japanese population |
title_sort | no association between bdnf val66met polymorphism and treatment response in obsessive-compulsive disorder in the japanese population |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4795591/ https://www.ncbi.nlm.nih.gov/pubmed/27042072 http://dx.doi.org/10.2147/NDT.S102100 |
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