Association between the Alu Insertion/Deletion Polymorphism in the Tissue-Type Plasminogen Activator Gene and Mirtazapine Response in Koreans with Major Depression.
- Author:
Daseul KIM
1
;
Hun Soo CHANG
;
Eunsoo WON
;
Byung Joo HAM
;
Min Soo LEE
Author Information
1. Department of Psychiatry, Korea University Anam Hospital, Korea University College of Medicine, Seoul, Korea. leeminso@korea.ac.kr
- Publication Type:Original Article
- Keywords:
Major depressive disorder;
Tissue type plasminogen activator;
Alu insertion/deletion;
Genetic polymorphism;
Mirtazapine treatment response
- MeSH:
Alleles;
Depression*;
Depressive Disorder, Major;
Genetic Markers;
Homozygote;
Humans;
Polymorphism, Genetic;
Tissue Plasminogen Activator*
- From:Journal of the Korean Society of Biological Psychiatry
2016;23(4):140-147
- CountryRepublic of Korea
- Language:Korean
-
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.
