No association between the response to the addition of an atypical antipsychotic drug to an selective serotonin reuptake inhibitor or serotonin norepinephrine reuptake inhibitor and the brain-derived neurotrophic factor (Val66Met) polymorphism in refractory major depressive disorder in Japanese patients

Reiji Yoshimura, Taro Kishi, Hikaru Hori, Atsuko Ikenouchi-Sugita, Wakako Umene-Nakano, Asuka Katsuki, Kenji Hayashi, Nakao Iwata, Jun Nakamura

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Abstract

Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population. Copyright

Original languageEnglish
Pages (from-to)49-53
Number of pages5
JournalClinical Psychopharmacology and Neuroscience
Volume10
Issue number1
DOIs
Publication statusPublished - 01-01-2012

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Brain-Derived Neurotrophic Factor
Major Depressive Disorder
Serotonin Uptake Inhibitors
Antipsychotic Agents
Treatment-Resistant Depressive Disorder
Drug Combinations
Serotonin and Noradrenaline Reuptake Inhibitors
Serum
Diagnostic and Statistical Manual of Mental Disorders
Antidepressive Agents
Therapeutics
Enzyme-Linked Immunosorbent Assay
Depression
Population

All Science Journal Classification (ASJC) codes

  • Psychiatry and Mental health
  • Behavioral Neuroscience
  • Pharmacology (medical)

Cite this

@article{644042b7aee843cea2dc2086b6500f43,
title = "No association between the response to the addition of an atypical antipsychotic drug to an selective serotonin reuptake inhibitor or serotonin norepinephrine reuptake inhibitor and the brain-derived neurotrophic factor (Val66Met) polymorphism in refractory major depressive disorder in Japanese patients",
abstract = "Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50{\%} over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50{\%} decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52{\%}) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population. Copyright",
author = "Reiji Yoshimura and Taro Kishi and Hikaru Hori and Atsuko Ikenouchi-Sugita and Wakako Umene-Nakano and Asuka Katsuki and Kenji Hayashi and Nakao Iwata and Jun Nakamura",
year = "2012",
month = "1",
day = "1",
doi = "10.9758/cpn.2012.10.1.49",
language = "English",
volume = "10",
pages = "49--53",
journal = "Clinical Psychopharmacology and Neuroscience",
issn = "1738-1088",
publisher = "Korean College of Neuropsychopharmacology",
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TY - JOUR

T1 - No association between the response to the addition of an atypical antipsychotic drug to an selective serotonin reuptake inhibitor or serotonin norepinephrine reuptake inhibitor and the brain-derived neurotrophic factor (Val66Met) polymorphism in refractory major depressive disorder in Japanese patients

AU - Yoshimura, Reiji

AU - Kishi, Taro

AU - Hori, Hikaru

AU - Ikenouchi-Sugita, Atsuko

AU - Umene-Nakano, Wakako

AU - Katsuki, Asuka

AU - Hayashi, Kenji

AU - Iwata, Nakao

AU - Nakamura, Jun

PY - 2012/1/1

Y1 - 2012/1/1

N2 - Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population. Copyright

AB - Objective: This study examined the association between the brain-derived neurotrophic factor (BDNF) (Val66Met) polymorphism and the response to the addition of an atypical antipsychotic drug to a selective serotonin reuptake inhibitor (SSRI) or serotonin-norepinephrine reuptake inhibitor (SNRI) in treatment-refractory depression. Methods: The study enrolled 64 patients meeting the Diagnostic and Statistical Manual of Mental Disorders-IV criteria for major depressive disorder who were treated with at least two courses of a single antidepressant, but who had Hamilton Depression Rating Scale (HAMD-17) scores ≥15 points that were reduced less than 50% over at least a 4-week treatment period. There were 24 males and 40 females (age range 27-68 years; mean±SD, 48±13 years). The patients' clinical improvement was evaluated using the HAMD-17. Patients with at least a 50% decrease in the HAMD-17 score were defined as responders. Serum BDNF levels were assayed using enzyme-linked immunosorbent assays and the presence of the BDNF (Val66Met) polymorphism was determined using the TaqMan genotyping assay. Results: No correlation was found between the BDNF (Val66Met) polymorphism and a positive response to adding an atypical antipsychotic drug. No differences were observed in the changes in the serum BDNF levels and HAMD-17 scores between Val66Val and Met-carriers. In addition, in patients who experienced remission, the atypical antipsychotic drug was discontinued after at least 3 months of treatment and the patients were then followed for 1 year; 14 of 27 patients (52%) relapsed within 1 year. Conclusion: These results suggest that the BDNF (Val66Met) polymorphism is not associated with the response to the augmentation of a SSRI or SNRI with an atypical antipsychotic drug, and that the combination of an atypical antipsychotic drug and a SSRI or SNRI should be continued for 3 months or more in refractory depressed patients in the Japanese population. Copyright

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