Monoamine oxidase: A gene polymorphism, tryptophan hydroxylase gene polymorphism and antidepressant response to fluvoxamine in Japanese patients with major depressive disorder

Yoshida, Keizo; Naito, Shokichi; Takahashi, Hitoshi; Sato, Kazuhiro; Ito, Kenichi; Kamata, Mitsuhiro; Higuchi, Hisashi; Shimizu, Tetsuo; Itoh, Ken; Inoue, Ken‐ichiro; Tezuka, Takehiko; Suzuki, Toshio; Ohkubo, Tadashi; Sugawara, Kazunobu; Otani, Koichi

doi:10.1016/s0278-5846(02)00267-1

Cited by 85 publications

(55 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The result also demonstrated significant differences between the two groups (w 2 ¼ 10.7,2, df ¼ 1, p ¼ 0.001) with 4R carriers more common in the MDD group. In this study, the MAOA-uVNTR allele frequency is different for this Chinese population as compared to European-American samples; however, our results are similar to the Japanese analog in which a high 3R allele frequency was demonstrated (3R allele frequency of control group: 65.9% in this study, 60% in the Japanese sample, and 25-38% in the European-American samples; 3R repeats allele frequency of major depressive group: 52.6% in this study, 58.4-59% in the Japanese sample, and 32% in the European-American samples) (Samochowiec et al, 2004;Schulze et al, 2000;Kunugi et al, 1999;Yoshida et al, 2002b).…”

Section: Resultssupporting

confidence: 85%

“…This polymorphism is functional in that 3.5R or 4R transcribed 2-10 times more efficiently than those with 2, 3, or 5R (Sabol et al, 1998). Although there are several negative association studies between MAOA-uVNTR gene polymorphism and psychiatric phenotype (Furlong et al, 1999;Yoshida et al, 2002b;Kunugi et al, 1999;Syagailo et al, 2001;Garpenstrand et al, 2002) including an alcoholism study in Han Chinese males (Lu et al, 2002), previous reports demonstrated that this polymorphism may be associated with monoamine metabolite concentrations in the CSF of healthy volunteers (Jonsson et al, 2000) as well as psychiatric diseases such as panic disorder (Deckert et al, 1999), obsessive-compulsive disorder (Camarena et al, 1998), bipolar disorder (Preisig et al, 2000), Alzheimer's disease (Takehashi et al, 2002), and schizophrenia (Jonsson et al, 2003). Considering the possible role of MAOA in the pathogenesis and therapeutic mechanisms, in this study, we investigated the possible association of the MAOA-uVNTR polymorphism with MDD and its antidepressant therapeutic response.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Yu¹,

Tsai

Hong

et al. 2005

Neuropsychopharmacol

161

122

View full text Add to dashboard Cite

Monoamine oxidase A (MAOA), a mitochondrial enzyme involved in the degradation of biogenic amines, may be implicated in the pathogenesis of major depressive disorder (MDD) and be related to the therapeutic effects of antidepressants. To elucidate a genetic predisposition of MDD, we studied a variable-number-tandem-repeat (VNTR) polymorphism in the promoter region of the MAOA gene in a Chinese population of 230 MDD patients and 217 controls. We also examined the association of this polymorphism and antidepressant therapeutic response in the MDD patients who underwent a 4-week fluoxetine treatment. Our results showed a significantly increased frequency of 4-repeat (4R) allele in MDD patients, especially in the female population. Furthermore, MDD female patients who were 3R homozygotes had a significantly better response to 4-week fluoxetine treatment when compared to 4R carriers (p ¼ 0.024), but there was a nonsignificant difference found in male patients (p ¼ 0.081). Since the 4R allele transcribed 2-10 times more efficiently than those with 3R allele, our findings suggest that the MAOA-uVNTR may be involved in the pathogenesis of MDD and the antidepressant therapeutic mechanisms in Chinese population, and that there may be a gender effect in this association.

show abstract

Section: Resultssupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Yu¹,

Tsai

Hong

et al. 2005

Neuropsychopharmacol

161

122

View full text Add to dashboard Cite

show abstract

“…The TPH to 5OH-TPH conversion the ratelimiting step in the conversion of serotonin, and polymorphisms have been found in both the TPH1 and TPH2 genes (Breidenthal et al, 2004;Nielsen et al, 1997). Evidence is inconsistent for the involvement of a common TPH1 SNP (A218C) in SSRI treatment response (Serretti et al, 2001;Yoshida et al, 2002) with no studies to date done to investigate treatment response and TPH2, which has been argued to be responsible for 5HT formation in the brain (Shaltiel et al, 2005). Certainly, other genes with noted SNPs may play a role in SSRI tolerability in the context of sexual dysfunction (eg monoamine oxidase A or nitric oxide synthase).…”

Section: Discussionmentioning

confidence: 99%

Serotonin 2A −1438 G/A and G-Protein Beta3 Subunit C825T Polymorphisms in Patients with Depression and SSRI-Associated Sexual Side-Effects

Bishop

Moline

Ellingrod

et al. 2006

Neuropsychopharmacol

View full text Add to dashboard Cite

The occurrence of sexual side-effects from antidepressants is thought to be mediated through serotonin 2A (5HT2A) receptors. It is currently unknown if functional polymorphisms in the 5HT2A receptor or its G-protein second messenger complex are related to sexual dysfunction in patients taking an selective serotonin reuptake inhibitor (SSRI) for depression. The purpose of this study was to determine the relationship of the 5HT2A À1438 G/A and GNB3 C825T single nucleotide polymorphisms with overall sexual well-being and individual components of sexual health as measured by the Changes in Sexual Functioning Questionnaire (CSFQ). We evaluated 89 outpatients (18-40 years of age) at low risk for other causes of sexual dysfunction who were being treated for depression with an SSRI and did not have sexual difficulties before taking the antidepressant. Outcome measures were stratified by 5HT2A and GNB3 genotypes. After controlling for age, gender, anxiety scale scores, and depression scale scores, persons with a GG genotype of the 5HT2A À1438 single nucleotide polymorphisms (SNP) were significantly more likely to be categorized as having sexual dysfunction than persons with a GA or AA genotype (OR ¼ 3.6; 95% CI 1.03, 12.6; p ¼ 0.046). Furthermore, the 5HT2A À1438 GG genotype was a significant predictor of lower arousal scores (p ¼ 0.022) after accounting for other measures. There was no significant relationship between any outcome measure and GNB3 genotype.

show abstract

“…24 Recently, the same polymorphism was investigated with monoamine oxidase A (MAOA)-variable number tandem repeat (VNTR) in 66 Japanese patients with a major depressive disorder during a 6-week controlled study. Only 54 patients completed the study, and they failed to demonstrate the association of the two polymorphisms with the antidepressant effect of fluvoxamine; 25 however, it must be observed that the sample was smaller than those of the previous studies and belonging to a different ethnicity. The same Japanese group also published a paper reporting the lack of association between this and other polymorphisms with the development of fluvoxamine-induced nausea.…”

Section: Candidate Genes Tryptophan Hydroxylase (Tph)mentioning

confidence: 85%

“…A recent study found no association between the same polymorphism and AD response to fluvoxamine in a Japanese sample. 25 Our group tested the association between fluvoxamine and paroxetine efficacy in a sample of 248 unipolar and 195 bipolar depressed patients, with or without psychotic features. 307 inpatients were treated with 300 mg fluvoxamine and 136 with 20-40 mg paroxetine for 6 weeks.…”

Section: Monoamine Oxidasementioning

confidence: 99%

The pharmacogenomics of selective serotonin reuptake inhibitors

Serretti

Artioli

2004

Pharmacogenomics J

View full text Add to dashboard Cite

The introduction of selective serotonin (5-HT) reuptake inhibitors (SSRIs) has significantly improved the pharmacological treatment of a range of psychiatric disorders. Nevertheless, despite the undoubted advantages of antidepressant treatment in terms of improved tolerability to therapy while maintaining a high level of efficacy, not all patients benefit from it; an appreciable proportion do not respond adequately, while others may show adverse reactions. The necessary change of the initial treatment choice often requires extended periods for the remission of symptomatology. Such difficulties could be avoided if it should be possible to determine more quickly the most suitable drug. Several factors have been thought to influence the outcome of antidepressant therapy. Among the factors influencing the interindividual variability in response to treatment with SSRI, differences in genetic features may play a significant role. Several genetic polymorphisms have been associated with therapeutic SSRI response, including genetic variants of the 5-HT transporter, 5-HT-2A-receptor, tryptophan hydroxylase, brain-derived neurotrophic factor, G-protein beta3 subunit, interleukin-1beta and angiotensin-converting enzyme, although with conflicting results; also cytochrome P450 drug-metabolising enzymes may bear a particular importance, although further corroboration of the findings is necessary, and further key participating genes remain to be identified. The hope is that the identification of these genetic components will eventually facilitate the development of a customised SSRI treatment. 1 These drugs show high efficacy, and relatively few adverse reactions compared with the previously used tricyclic antidepressants, even though their mechanism of action is not entirely understood yet. However, these drugs are effective in only about two-thirds of depressed patients.2 The necessary change of the initial treatment choice often requires extended periods for the remission of symptomatology. Such difficulties could be avoided if it would be possible to determine more quickly the most suitable drug for each subject. Several factors have been thought to influence the outcome of antidepressant therapy and efficient clinical predictors have not been yet identified, but there is some evidence suggesting that genetic factors play a substantial role.

show abstract

Monoamine oxidase: A gene polymorphism, tryptophan hydroxylase gene polymorphism and antidepressant response to fluvoxamine in Japanese patients with major depressive disorder

Cited by 85 publications

References 16 publications

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Association Study of a Monoamine Oxidase A Gene Promoter Polymorphism with Major Depressive Disorder and Antidepressant Response

Serotonin 2A −1438 G/A and G-Protein Beta3 Subunit C825T Polymorphisms in Patients with Depression and SSRI-Associated Sexual Side-Effects

The pharmacogenomics of selective serotonin reuptake inhibitors

Contact Info

Product

Resources

About