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2015 Fiscal Year Final Research Report

New therapeutic strategy for major depression based on anti-inflammatory action of antidepressants and application to personalized medicine

Research Project

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Project/Area Number 25460650
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Applied pharmacology
Research InstitutionNagasaki University

Principal Investigator

TSUKAMOTO Kazuhiro  長崎大学, 医歯薬学総合研究科(薬学系), 教授 (30253305)

Co-Investigator(Renkei-kenkyūsha) KUROTAKI Naohiro  長崎大学, 医歯薬学総合研究科(医学系), 准教授 (20423634)
Research Collaborator NISHIWAKI Kenzaburo  
KOJIMA Ryoko  
KUROKAWA Takuya  
ARAKI Chizuru  
ARATA Yuki  
SHIMOMIYAZONO Aya  
KEYA Koji  
OBATA Kyosuke  
KAWAFUCHI Yuka  
IJICHI Shunsuke  
TANIGUCHI Shunsuke  
NISHIZONO Miki  
Project Period (FY) 2013-04-01 – 2016-03-31
Keywordsうつ病 / 抗うつ薬 / 薬剤応答性遺伝子 / うつ病の病因論 / 相関解析 / 遺伝子診断 / ゲノム創薬
Outline of Final Research Achievements

Neuroinflammation and neuroplasticity contribute to the pathogenesis of major depression (MD) as well as response to antidepressant(s). In this study, in order to identify responsibility genes to antidepressant, we examined an association between polymorphisms of 161 single nucleotide polymorphisms in the 34 candidate genes and the therapeutic effect of antidepressant (SSRI or SNRI) at the period of 8-week treatment using 105 Japanese MD patients. We identified 9 SSRI-resistant responsibility genes and 2 SNRI-resistant responsibility genes.
Genetic test revealed that the best combination of polymorphisms of FRS3 and RET is useful as a biomarker for identifying non-responders to SSRI after 8-weeks treatment. Moreover, since the dual-luciferase assay showed the difference in transcriptional activity between C allele and G allele of rs1061624 in TNFRSF1B in Jurkat cells, this receptor may become a target molecule for a novel drug against SSRI-resistant MD patients.

Free Research Field

分子遺伝学

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Published: 2017-05-10  

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