Pharmacogenetic study of serotonin 6 receptor gene with antidepressant response in major depressive disorder in the Japanese population

2010 ◽  
Vol 25 (6) ◽  
pp. 481-486 ◽  
Author(s):  
Taro Kishi ◽  
Yasuhisa Fukuo ◽  
Reiji Yoshimura ◽  
Tomo Okochi ◽  
Tsuyoshi Kitajima ◽  
...  
CNS Spectrums ◽  
2012 ◽  
Vol 17 (2) ◽  
pp. 76-86 ◽  
Author(s):  
David Mischoulon ◽  
Stefania Lamon-Fava ◽  
Jacob Selhub ◽  
Judith Katz ◽  
George I. Papakostas ◽  
...  

AbstractObjectiveTo examine the prevalence of the C677T polymorphism of the methylene tetrahydrofolate reductase (MTHFR) gene and the A2756G polymorphism of methionine synthase (MS), and their impact on antidepressant response.MethodsWe screened 224 subjects (52% female, mean age 39 ± 11 years) with SCID-diagnosed major depressive disorder (MDD), and obtained 194 genetic samples. 49 subjects (49% female, mean age 36 ± 11 years) participated in a 12-week open clinical trial of fluoxetine 20–60 mg/day. Association between clinical response and C677T and A2756G polymorphisms, folate, B12, and homocysteine was examined.ResultsPrevalence of the C677T and A2756G polymorphisms was consistent with previous reports (C/C = 41%, C/T = 47%, T/T = 11%, A/A = 66%, A/G = 29%, G/G = 4%). In the fluoxetine-treated subsample (n = 49), intent-to-treat (ITT) response rates were 47% for C/C subjects and 46% for pooled C/T and T/T subjects (nonsignificant). ITT response rates were 38% for A/A subjects and 60% for A/G subjects (nonsignificant), with no subjects exhibiting the G/G homozygote. Mean baseline plasma B12 was significantly lower in A/G subjects compared to A/A, but folate and homocysteine levels were not affected by genetic status. Plasma folate was negatively associated with treatment response.ConclusionThe C677T and A2756G polymorphisms did not significantly affect antidepressant response. These preliminary findings require replication in larger samples.


2020 ◽  
Vol 25 ◽  
pp. 102178
Author(s):  
Jee Su Suh ◽  
Luciano Minuzzi ◽  
Pradeep Reddy Raamana ◽  
Andrew Davis ◽  
Geoffrey B. Hall ◽  
...  

2018 ◽  
Vol 83 (9) ◽  
pp. S399
Author(s):  
Crystal Cooper ◽  
Cherise Chin Fatt ◽  
Gregory Fonzo ◽  
Manish Jha ◽  
Bruce Grannemann ◽  
...  

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Shiyi Xie ◽  
Yan Hu ◽  
Li Fang ◽  
Shijia Chen ◽  
Benson O.A. Botchway ◽  
...  

Abstract Major depressive disorder is a genetic susceptible disease, and a psychiatric syndrome with a high rate of incidence and recurrence. Because of its complexity concerning etiology and pathogenesis, the cure rate of first-line antidepressants is low. In recent years, accumulative evidences revealed that oxytocin act as a physiological or pathological participant in a variety of complex neuropsychological activities, including major depressive disorder. Six electronic databases (Web of Science, PubMed, Scopus, Google Scholar, CNKI, and Wanfang) were employed for researching relevant publications. At last, 226 articles were extracted. The current review addresses the correlation of the oxytocin system and major depressive disorder. Besides, we summarize the mechanisms by which the oxytocin system exerts potential antidepressant effects, including regulating neuronal activity, influencing neuroplasticity and regeneration, altering neurotransmitter release, down regulating hypothalamic–pituitary–adrenal axis, anti-inflammatory, antioxidation, and genetic effects. Increasing evidence shows that oxytocin and its receptor gene may play a potential role in major depressive disorder. Future research should focus on the predictive ability of the oxytocin system as a biomarker, as well as its role in targeted prevention and early intervention of major depressive disorder.


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