SIRT1 gene is associated with major depressive disorder in the Japanese population

Taro Kishi, Reiji Yoshimura, Tsuyoshi Kitajima, Tomo Okochi, Takenori Okumura, Tomoko Tsunoka, Yoshio Yamanouchi, Yoko Kinoshita, Kunihiro Kawashima, Yasuhisa Fukuo, Hiroshi Naitoh, Wakako Umene-Nakano, Toshiya Inada, Jun Nakamura, Norio Ozaki, Nakao Iwata

Research output: Contribution to journalArticle

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Abstract

Background: Many studies including our previous ones as to PROKR2 and CLOCK have suggested that circadian genes may be involved in the mechanisms of mood disorders and their treatment responses. Also several recent investigations have reported that SIRT1 plays an important role in the circadian system as conventional circadian clock genes, and also have some relation to dopaminergic metabolism. So we considered the SIRT1 gene to be a good candidate gene for the pathophysiology for MDD and SSRI responses in MDD, and conducted a case-control study using four tagging SNPs (450 MDD patients, including 261 patients treated by SSRIs and 766 controls). Method: The MDD patients in this study had scores of 12 or higher on the 17 items of the Structured Interview Guide for Hamilton Rating Scale for Depression (SIGH-D). We defined a clinical response as a decrease of more than 50% in baseline SIGH-D within 8 weeks, and clinical remission as an SIGH-D score of less than 7 at 8 weeks. Marker-trait association analysis was used to evaluate allele and genotype association with the chi-square test, and haplotype association analysis was evaluated with a likelihood ratio test. Result: We found an association between rs10997875 in SIRT1 gene and MDD in the allele/genotype analysis. In addition, this significance of these associations survived Bonferroni correction. However, we did not find any association between SIRT1 gene and SSRI therapeutic response in MDD in the allele/genotype analysis or haplotype analysis. Limitations: A replication study using larger samples may be required for conclusive results, since our sample size was small. Conclusions: Our results suggest that rs10997875 in SIRT1 gene may play a role in the pathophysiology of MDD in the Japanese population.

Original languageEnglish
Pages (from-to)167-173
Number of pages7
JournalJournal of Affective Disorders
Volume126
Issue number1-2
DOIs
Publication statusPublished - 01-10-2010

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Major Depressive Disorder
Population
Genes
Alleles
Genotype
Haplotypes
Circadian Clocks
Chi-Square Distribution
Mood Disorders
Sample Size
Single Nucleotide Polymorphism
Case-Control Studies
Interviews
Depression
Therapeutics

All Science Journal Classification (ASJC) codes

  • Clinical Psychology
  • Psychiatry and Mental health

Cite this

Kishi, Taro ; Yoshimura, Reiji ; Kitajima, Tsuyoshi ; Okochi, Tomo ; Okumura, Takenori ; Tsunoka, Tomoko ; Yamanouchi, Yoshio ; Kinoshita, Yoko ; Kawashima, Kunihiro ; Fukuo, Yasuhisa ; Naitoh, Hiroshi ; Umene-Nakano, Wakako ; Inada, Toshiya ; Nakamura, Jun ; Ozaki, Norio ; Iwata, Nakao. / SIRT1 gene is associated with major depressive disorder in the Japanese population. In: Journal of Affective Disorders. 2010 ; Vol. 126, No. 1-2. pp. 167-173.
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abstract = "Background: Many studies including our previous ones as to PROKR2 and CLOCK have suggested that circadian genes may be involved in the mechanisms of mood disorders and their treatment responses. Also several recent investigations have reported that SIRT1 plays an important role in the circadian system as conventional circadian clock genes, and also have some relation to dopaminergic metabolism. So we considered the SIRT1 gene to be a good candidate gene for the pathophysiology for MDD and SSRI responses in MDD, and conducted a case-control study using four tagging SNPs (450 MDD patients, including 261 patients treated by SSRIs and 766 controls). Method: The MDD patients in this study had scores of 12 or higher on the 17 items of the Structured Interview Guide for Hamilton Rating Scale for Depression (SIGH-D). We defined a clinical response as a decrease of more than 50{\%} in baseline SIGH-D within 8 weeks, and clinical remission as an SIGH-D score of less than 7 at 8 weeks. Marker-trait association analysis was used to evaluate allele and genotype association with the chi-square test, and haplotype association analysis was evaluated with a likelihood ratio test. Result: We found an association between rs10997875 in SIRT1 gene and MDD in the allele/genotype analysis. In addition, this significance of these associations survived Bonferroni correction. However, we did not find any association between SIRT1 gene and SSRI therapeutic response in MDD in the allele/genotype analysis or haplotype analysis. Limitations: A replication study using larger samples may be required for conclusive results, since our sample size was small. Conclusions: Our results suggest that rs10997875 in SIRT1 gene may play a role in the pathophysiology of MDD in the Japanese population.",
author = "Taro Kishi and Reiji Yoshimura and Tsuyoshi Kitajima and Tomo Okochi and Takenori Okumura and Tomoko Tsunoka and Yoshio Yamanouchi and Yoko Kinoshita and Kunihiro Kawashima and Yasuhisa Fukuo and Hiroshi Naitoh and Wakako Umene-Nakano and Toshiya Inada and Jun Nakamura and Norio Ozaki and Nakao Iwata",
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Kishi, T, Yoshimura, R, Kitajima, T, Okochi, T, Okumura, T, Tsunoka, T, Yamanouchi, Y, Kinoshita, Y, Kawashima, K, Fukuo, Y, Naitoh, H, Umene-Nakano, W, Inada, T, Nakamura, J, Ozaki, N & Iwata, N 2010, 'SIRT1 gene is associated with major depressive disorder in the Japanese population', Journal of Affective Disorders, vol. 126, no. 1-2, pp. 167-173. https://doi.org/10.1016/j.jad.2010.04.003

SIRT1 gene is associated with major depressive disorder in the Japanese population. / Kishi, Taro; Yoshimura, Reiji; Kitajima, Tsuyoshi; Okochi, Tomo; Okumura, Takenori; Tsunoka, Tomoko; Yamanouchi, Yoshio; Kinoshita, Yoko; Kawashima, Kunihiro; Fukuo, Yasuhisa; Naitoh, Hiroshi; Umene-Nakano, Wakako; Inada, Toshiya; Nakamura, Jun; Ozaki, Norio; Iwata, Nakao.

In: Journal of Affective Disorders, Vol. 126, No. 1-2, 01.10.2010, p. 167-173.

Research output: Contribution to journalArticle

TY - JOUR

T1 - SIRT1 gene is associated with major depressive disorder in the Japanese population

AU - Kishi, Taro

AU - Yoshimura, Reiji

AU - Kitajima, Tsuyoshi

AU - Okochi, Tomo

AU - Okumura, Takenori

AU - Tsunoka, Tomoko

AU - Yamanouchi, Yoshio

AU - Kinoshita, Yoko

AU - Kawashima, Kunihiro

AU - Fukuo, Yasuhisa

AU - Naitoh, Hiroshi

AU - Umene-Nakano, Wakako

AU - Inada, Toshiya

AU - Nakamura, Jun

AU - Ozaki, Norio

AU - Iwata, Nakao

PY - 2010/10/1

Y1 - 2010/10/1

N2 - Background: Many studies including our previous ones as to PROKR2 and CLOCK have suggested that circadian genes may be involved in the mechanisms of mood disorders and their treatment responses. Also several recent investigations have reported that SIRT1 plays an important role in the circadian system as conventional circadian clock genes, and also have some relation to dopaminergic metabolism. So we considered the SIRT1 gene to be a good candidate gene for the pathophysiology for MDD and SSRI responses in MDD, and conducted a case-control study using four tagging SNPs (450 MDD patients, including 261 patients treated by SSRIs and 766 controls). Method: The MDD patients in this study had scores of 12 or higher on the 17 items of the Structured Interview Guide for Hamilton Rating Scale for Depression (SIGH-D). We defined a clinical response as a decrease of more than 50% in baseline SIGH-D within 8 weeks, and clinical remission as an SIGH-D score of less than 7 at 8 weeks. Marker-trait association analysis was used to evaluate allele and genotype association with the chi-square test, and haplotype association analysis was evaluated with a likelihood ratio test. Result: We found an association between rs10997875 in SIRT1 gene and MDD in the allele/genotype analysis. In addition, this significance of these associations survived Bonferroni correction. However, we did not find any association between SIRT1 gene and SSRI therapeutic response in MDD in the allele/genotype analysis or haplotype analysis. Limitations: A replication study using larger samples may be required for conclusive results, since our sample size was small. Conclusions: Our results suggest that rs10997875 in SIRT1 gene may play a role in the pathophysiology of MDD in the Japanese population.

AB - Background: Many studies including our previous ones as to PROKR2 and CLOCK have suggested that circadian genes may be involved in the mechanisms of mood disorders and their treatment responses. Also several recent investigations have reported that SIRT1 plays an important role in the circadian system as conventional circadian clock genes, and also have some relation to dopaminergic metabolism. So we considered the SIRT1 gene to be a good candidate gene for the pathophysiology for MDD and SSRI responses in MDD, and conducted a case-control study using four tagging SNPs (450 MDD patients, including 261 patients treated by SSRIs and 766 controls). Method: The MDD patients in this study had scores of 12 or higher on the 17 items of the Structured Interview Guide for Hamilton Rating Scale for Depression (SIGH-D). We defined a clinical response as a decrease of more than 50% in baseline SIGH-D within 8 weeks, and clinical remission as an SIGH-D score of less than 7 at 8 weeks. Marker-trait association analysis was used to evaluate allele and genotype association with the chi-square test, and haplotype association analysis was evaluated with a likelihood ratio test. Result: We found an association between rs10997875 in SIRT1 gene and MDD in the allele/genotype analysis. In addition, this significance of these associations survived Bonferroni correction. However, we did not find any association between SIRT1 gene and SSRI therapeutic response in MDD in the allele/genotype analysis or haplotype analysis. Limitations: A replication study using larger samples may be required for conclusive results, since our sample size was small. Conclusions: Our results suggest that rs10997875 in SIRT1 gene may play a role in the pathophysiology of MDD in the Japanese population.

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DO - 10.1016/j.jad.2010.04.003

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JF - Journal of Affective Disorders

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