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Brain-derived neurotrophic factor gene polymorphisms and mirtazapine responses in Koreans with major depression

Authors
Kang, R. H.Chang, H. S.Wong, M. L.Choi, M. J.Park, J. Y.Lee, H. Y.Jung, I. K.Joe, S. H.Kim, L.Kim, S. H.Kim, Y. K.Han, C. S.Ham, B. J.Lee, H. J.Ko, Y. H.Lee, M. S.Lee, M. S.
Issue Date
Dec-2010
Publisher
SAGE PUBLICATIONS LTD
Keywords
brain-derived neurotrophic factor; gene polymorphisms; major depression; mirtazapine; treatment response
Citation
JOURNAL OF PSYCHOPHARMACOLOGY, v.24, no.12, pp.1755 - 1763
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF PSYCHOPHARMACOLOGY
Volume
24
Number
12
Start Page
1755
End Page
1763
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/115142
DOI
10.1177/0269881109105457
ISSN
0269-8811
Abstract
Brain-derived neurotrophic factor (BDNF) is a candidate molecule for influencing the clinical response to antidepressant treatment. The aims of this study were to determine the relationship between the Val66Met polymorphism in the BDNF gene and the response to mirtazapine in 243 Korean subjects with major depressive disorder (MDD). The reduction in the Hamilton Depression score over the 8-week treatment period was not influenced by BDNF V66M genotypes. A marginal effect of genotype on somatic anxiety score was observed at baseline (P = 0.047 in the dominant model). However, genotype-time interaction had no effect on somatic anxiety score after the 8-week a treatment period. Plasma BDNF levels tended to increase during mirtazapine treatment, although without statistical significance (P = 0.055). After 8 weeks of mirtazapine treatment, plasma BDNF levels were higher in Met allele homozygotes (1499.7 +/- 370.6 ng/mL) than in Val allele carriers (649.7 +/- 158.5 ng/mL, P = 0.049). Our results do not support the hypothesis that the Val66Met promoter polymorphism in the BDNF gene influences the therapeutic response to mirtazapine in Korean MDD patients. However, our data indicate that this polymorphism results in increased plasma BDNF after mirtazapine treatment.
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