title: The G196A polymorphism of the brain-derived neurotrophic factor gene and the antidepressant effect of milnacipran and fluvoxamine.
abstract: Prediction of the response to different classes of antidepressants has been an important matter of concern in the field of psychopharmacology. The purpose of the present study was to investigate whether the G196A polymorphism of the brain-derived neurotrophic factor (BDNF) gene is associated with the antidepressant effect of milnacipran, a serotonin norepinephrine reuptake inhibitor, and fluvoxamine, a selective serotonin reuptake inhibitor. The subjects of our previous study of milnacipran (n = 80) and fluvoxamine (n = 54) were included in the present study. Severity of depression was assessed with the Montgomery Asberg depression rating scale (MADRS). Assessments were carried out at baseline and at 1, 2, 4 and 6 weeks of treatment. Polymerase chain reaction was used to determine allelic variants. In all subjects receiving milnacipran or fluvoxamine, the G/A genotype of the BDNF G196A polymorphism was associated with a significantly better therapeutic effect in the MADRS scores during this study. When milnacipran and fluvoxamine-treated subjects were analysed independently, the G/A genotype group showed greater reduction of MADRS scores than other genotype groups, irrespective of which antidepressant was administered. These results suggest that the BDNF G196A polymorphism in part determines the antidepressant effect of both milnacipran and fluvoxamine.
authors.affiliation: Department of Psychiatry, Nagoya University Graduate School of Medicine, 65 Tsurumail-cho, Showa-ku, Nagoya, Aichi 466-8550, Japan. cxw01076@nifty.com
authors.forename: Keizo
authors.initials: K
authors.lastname: Yoshida
authors.forename: Hisashi
authors.initials: H
authors.lastname: Higuchi
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Kamata
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Takahashi
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Inoue
authors.forename: Toshio
authors.initials: T
authors.lastname: Suzuki
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Itoh
authors.forename: Norio
authors.initials: N
authors.lastname: Ozaki
mesh_terms: D000328:Adult; D000928:Antidepressive Agents / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics*; D003521:Cyclopropanes / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D003863:Depression / Q000188:drug therapy* / Q000235:genetics; D005091:Exons; D005260:Female; D016666:Fluvoxamine / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D000078764:Milnacipran; D010349:Patient Compliance; D018579:Patient Selection; D010641:Phenotype; D011110:Polymorphism, Genetic; D017367:Selective Serotonin Reuptake Inhibitors / Q000097:blood / Q000493:pharmacokinetics / Q000627:therapeutic use*; D012720:Severity of Illness Index; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000928:Antidepressive Agents; D019208:Brain-Derived Neurotrophic Factor; D003521:Cyclopropanes; D016666:Fluvoxamine; D000078764:Milnacipran; D017367:Selective Serotonin Reuptake Inhibitors