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 Refracto.
- Author:
Reiji YOSHIMURA
1
;
Taro KISHI
;
Hikaru HORI
;
Atsuko IKENOUCHI-SUGITA
;
Wakako UMENE-NAKANO
;
Asuka KATSUKI
;
Kenji HAYASHI
;
Nakao IWATA
;
Jun NAKAMURA
Author Information
1. Department of Psychiatry, University of Occupational and Environmental Health, Kitakyushu, Japan. yoshi621@med.uoeh-u.ac.jp
- Publication Type:Original Article
- Keywords:
Brain-derived neurotrophic factor;
Treatment-resistant depressive disorder;
Antipsychotic drug;
Polymorphism;
Selective Serotonin Reuptake Inhibitor;
Serotonin Norepinephrine Reuptake Inhibitor
- MeSH:
Asian Continental Ancestry Group;
Brain-Derived Neurotrophic Factor;
Depression;
Depressive Disorder, Major;
Depressive Disorder, Treatment-Resistant;
Enzyme-Linked Immunosorbent Assay;
Female;
Humans;
Male;
Norepinephrine;
Serotonin
- From:Clinical Psychopharmacology and Neuroscience
2012;10(1):49-53
- CountryRepublic of Korea
- Language:English
-
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 > or =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.
