Evidence for association between genetic variants of p75 neurotrophin receptor (p75NTR) gene and antidepressant treatment response in chinese major depressive disorder

Gau, Yung‐Tian A.; Liou, Ying‐Jay; Yu, Younger W.‐Y.; Chen, Tai‐Jui; Lin, Ming‐Wei; Tsai, Shih‐Jen

doi:10.1002/ajmg.b.30646

Cited by 26 publications

(15 citation statements)

References 34 publications

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“…Evidence in support of this hypothesis has been reported (e.g. DTN-BP1 and NGFR ) [16,17] . Therefore, although NR1D1 was not found to play a major key role in the pathophysiology of mood disorders [3] , we considered that NR1D1 might be a susceptibility gene for SSRI treatment response.…”

supporting

confidence: 61%

Orphan Nuclear Receptor Rev-erb Alpha Gene (NR1D1) and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Kishi

Kitajima²,

Ikeda³

et al. 2009

Neuropsychobiology

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Background: Sleep-wake disturbance, frequently observed in major depressive disorder (MDD), negatively influences clinical status. Treatment with antidepressants also reportedly affects circadian rhythms. In a recent in vitro study, the nuclear receptor Rev-erbα was reported to be related to circadian rhythms, and was shown to be involved in the biological action of lithium therapy. Therefore, we examined the association between the orphan nuclear receptor Rev-erbα gene (NR1D1) and the efficacy of fluvoxamine treatment in 118 Japanese patients with major depressive disorder. Methods: The scores of the MDD patients in this study on the 17 items of the Structured Interview Guide for the Hamilton Rating Scale for Depression (SIGH-D) were 12 or higher. We defined a clinical response as a decrease of more than 50% in baseline SIGH-D within 8 weeks and clinical remission as a SIGH-D score of less than 7 at 8 weeks. We selected 3 ‘tagging SNPs’ in NR1D1 for the following association analysis. Results: We did not detect a significant association between NR1D1 and the fluvoxamine therapeutic response in MDD in allele/genotype-wise analysis or haplotype-wise analysis. Conclusion: Our results suggest that NR1D1 does not play a major role in the therapeutic response to fluvoxamine in Japanese MDD patients. However, because our sample was small, a replication study using another population and a larger sample will be required for conclusive results.

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supporting

confidence: 61%

Orphan Nuclear Receptor Rev-erb Alpha Gene (NR1D1) and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Kishi

Kitajima²,

Ikeda³

et al. 2009

Neuropsychobiology

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“…As mentioned earlier, Gau et al (2008) failed to replicate the finding and discussed that the inconsistency of these results could be attributed from the intrinsic difference in the MDD subgroups and different ethnic groups. With respect to Ser205Leu, individual studies contained 164-670 patients with MDD and 164-1130 controls, and the combined sample consisted of 1060 patients and 1688 controls ( Table 2).…”

Section: Discussionmentioning

confidence: 86%

“…However, a subsequent study in a Han Chinese population failed to obtain evidence for the association. 7 This study tried to replicate the association in an independent larger sample. 8 on the basis of unstructured interviews and information from medical records.…”

Section: Introductionmentioning

confidence: 99%

Support for association between the Ser205Leu polymorphism of p75NTR and major depressive disorder

et al. 2011

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Altered neurotrophin functions have been implicated in major depressive disorder (MDD). Previously, we reported an association between MDD and a missense polymorphism (Ser205Leu: rs2072446) of the gene encoding the p75 neurotrophin receptor (p75 NTR ). However, contradictive negative results have also been reported. This study tried to replicate the association in an independent sample. Subjects were 668 patients with MDD and 1130 healthy controls. The proportion of individuals carrying the Leu205 allele was significantly decreased in the patients than in the controls (v 2 ¼5.3, d.f.¼1, P¼0.021, odds ratio (OR) 0.74, 95% confidential interval (CI) 0.58-0.96). When allele frequencies were compared, the Leu205 allele was significantly reduced in the patients than in the controls (v 2 ¼4.4, d.f.¼1, P¼0.037, OR 0.78, 95% CI 0.61-0.99). When men and women were examined separately, there was a significant difference in genotype and allele distributions in women (genotype: v 2 ¼8.3, d.f.¼1, P¼0.0039, OR 0.60, 95% CI 0.43-0.85; allele: v 2 ¼7.3, d.f.¼1, P¼0.0069, OR 0.64, 95% CI 0.47-0.89), but not in men. The present study provided support for the previously reported association between the Ser205Leu polymorphism of the p75 NTR gene and MDD, indicating that the Leu205 allele has a protective effect against the development of MDD, particularly in women.

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“…Future studies should consider genes in the BDNF signaling pathway, which may contribute or interact with BDNF in the response to antidepressant treatment. Recently, we found that one p75NTR missense polymorphism (S250L) was associated with the antidepressant response,53 and TrkB genetic variants may interact with the BDNF Val66Met polymorphism to contribute to the risk of geriatric depression 54. We also found that SNPs in glycogen synthase kinase-3beta ( GSK3B ), an important component in BDNF signaling, were associated with the therapeutic effects of antidepressants 55.…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Effects ofBDNFPolymorphisms on Antidepressant Action

Tsai

Hong

Liou

2010

Psychiatry Investig

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Evidence suggests that the down-regulation of the signaling pathway involving brain-derived neurotrophic factor (BDNF), a molecular element known to regulate neuronal plasticity and survival, plays an important role in the pathogenesis of major depression. The restoration of BDNF activity induced by antidepressant treatment has been implicated in the antidepressant therapeutic mechanism. Because there is variability among patients with major depressive disorder in terms of response to antidepressant treatment and since genetic factors may contribute to this inter-individual variability in antidepressant response, pharmacogenetic studies have tested the associations between genetic polymorphisms in candidate genes related to antidepressant therapeutic action. In human BDNF gene, there is a common functional polymorphism (Val66Met) in the pro-region of BDNF, which affects the intracellular trafficking of proBDNF. Because of the potentially important role of BDNF in the antidepressant mechanism, many pharmacogenetic studies have tested the association between this polymorphism and the antidepressant therapeutic response, but they have produced inconsistent results. A recent meta-analysis of eight studies, which included data from 1,115 subjects, suggested that the Val/Met carriers have increased antidepressant response in comparison to Val/Val homozygotes, particularly in the Asian population. The positive molecular heterosis effect (subjects heterozygous for a specific genetic polymorphism show a significantly greater effect) is compatible with animal studies showing that, although BDNF exerts an antidepressant effect, too much BDNF may have a detrimental effect on mood. Several recommendations are proposed for future antidepressant pharmacogenetic studies of BDNF, including the consideration of multiple polymorphisms and a haplotype approach, gene-gene interaction, a single antidepressant regimen, controlling for age and gender interactions, and pharmacogenetic effects on specific depressive symptom-clusters.

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Evidence for association between genetic variants of p75 neurotrophin receptor (p75^NTR) gene and antidepressant treatment response in chinese major depressive disorder

Cited by 26 publications

References 34 publications

Orphan Nuclear Receptor Rev-erb Alpha Gene <i>(NR1D1)</i> and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Orphan Nuclear Receptor Rev-erb Alpha Gene <i>(NR1D1)</i> and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Support for association between the Ser205Leu polymorphism of p75NTR and major depressive disorder

Effects ofBDNFPolymorphisms on Antidepressant Action

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