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Association between the Alu Insertion/Deletion Polymorphism in the Tissue-Type Plasminogen Activator Gene and Mirtazapine Response in Koreans with Major Depression  

Kim, Daseul (Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine)
Chang, Hun Soo (Department of Medical Bioscience, Soonchunhyang University)
Won, Eunsoo (Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine)
Ham, Byung-Joo (Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine)
Lee, Min-Soo (Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine)
Publication Information
Korean Journal of Biological Psychiatry / v.23, no.4, 2016 , pp. 140-147 More about this Journal
Abstract
Objectives To determine the relationship between the Alu insertion/deletion (I/D) polymorphism in the tissue-type plasminogen activator (tPA) gene and the clinical outcome of mirtazapine treatment in Korean major depressive disorder (MDD) patients. Methods We enrolled 422 patients in this study. Symptoms were evaluated using the 21-item Hamilton Depression Rating (HAMD-21) Scale. After 1, 2, 4, and 8 weeks of mirtazapine treatment, the association between the Alu I/D polymorphism in the tPA gene and remission/response outcomes were evaluated. Results The proportion of I/I homozygotes in responders was higher than that in non-responders, whereas the proportion of D/D homozygotes in responders was lower than that in non-responders at 8 weeks of treatment (p = 0.032, OR = 1.57). The percentage decline of HAMD-21 scores in I allele carriers was larger than that of D/D homozygotes at 2 and 8 weeks of treatment (p = 0.035 and 0.007, respectively). I allele carriers were associated with remission at 8 weeks of treatment (p = 0.047, OR = 2.2). Conclusions These results show that treatment response and remission to mirtazapine were associated with the Alu I/D polymorphism of the tPA gene. This suggests the Alu I/D polymorphism may be a potential genetic marker for the prediction of therapeutic response to mirtazapine treatment in patients with MDD.
Keywords
Major depressive disorder; Tissue type plasminogen activator; Alu insertion/deletion; Genetic polymorphism; Mirtazapine treatment response;
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