A splice site polymorphism in the G-protein β subunit influences antidepressant efficacy in depression

Wilkie, Murray J.V.; Smith, Daniel J.; Reid, Ian; Day, Richard; Matthews, Keith; Wolf, C. Roland; Blackwood, Douglas; Smith, Gillian

doi:10.1097/fpc.0b013e32801a3be6

Cited by 74 publications

(50 citation statements)

References 57 publications

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“…Genetic polymorphisms CREB1 polymorphisms have been associated with mood disorders, mainly exhibiting a significant gender effect (Zubenko et al 2003a(Zubenko et al , 2003bPerlis et al 2007;Dong et al 2009;Utge et al 2010;Juhasz et al 2011;Lazary et al 2011), nevertheless not unequivocally (Burcescu et al 2005;Hettema et al 2009). Findings for CREB1 and antidepressant response are also inconsistent (Murphy et al 2004;Wilkie et al 2007;Serretti et al 2011;Calati et al 2013) and negative findings have also been reported (Dong et al 2009;Crisafulli et al 2012;Matsumoto et al 2014).…”

Section: Cyclic Amp Response Element Binding Proteinmentioning

confidence: 78%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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Major depressive disorder (MDD) is a heritable disease with a heavy personal and socio-economic burden. Antidepressants of different classes are prescribed to treat MDD, but reliable and reproducible markers of efficacy are not available for clinical use. Further complicating treatment, the diagnosis of MDD is not guided by objective criteria, resulting in the risk of under-or overtreatment. A number of markers of MDD and antidepressant response have been investigated at the genetic, epigenetic, gene expression and protein levels. Polymorphisms in genes involved in anti-depressant metabolism (cytochrome P450 isoenzymes), antidepressant transport (ABCB1), glucocorticoid signalling (FKBP5) and serotonin neurotransmission (SLC6A4 and HTR2A) were among those included in the first pharmacogenetic assays that have been tested for clinical applicability. The results of these investigations were encouraging when examining patient-outcome improvement. Furthermore, a nine-serum biomarker panel (including BDNF, cortisol and soluble TNF-a receptor type II) showed good sensitivity and specificity in differentiating between MDD and healthy controls. These first diagnostic and response-predictive tests for MDD provided a source of optimism for future clinical applications. However, such findings should be considered very carefully because their benefit/cost ratio and clinical indications were not clearly demonstrated. Future tests may include combinations of different types of biomarkers and be specific for MDD subtypes or pathological dimensions.

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Section: Cyclic Amp Response Element Binding Proteinmentioning

confidence: 78%

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Fabbri

Hosák

Mößner

et al. 2016

The World Journal of Biological Psychiatry

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“…302 The GNB3 (825)T variant was found to predict a better antidepressant response in 5 independent studies. 170,[303][304][305][306] Lack of association has also been found. 83,307,308 Hypothalamic-pituitary-adrenal axis and stress hormone system Dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis is one of the most robust findings in many patients with MDD (up to 70%).…”

Section: Intracellular Signal Transduction Pathwaysmentioning

confidence: 95%

Pharmacogenetics of antidepressant response

Porcelli

Drago

Fabbri

et al. 2011

J Psychiatry Neurosci

156

103

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87Personalized medicine -the adaptation of therapies based on an individual's genetic and molecular profile -is one of the most promising aspects of modern medicine. The identification of the relation between genotype and drug response, including both the therapeutic effect and side effect profile, is expected to deeply affect medical practice. In this paper, we review the current knowledge about the genes related to antidepressant treatment response and provide methodologic proposals for future studies. We have mainly focused on genes associated with pharmacodynamics, for which a list of promising genes has been identified despite some inconsistency across studies. We have also synthesized the main results for pharmacokinetic genes, although so far they seem less relevant than those for pharmaco dynamic genes. We discuss possible reasons for these inconsistent findings and propose new study designs.

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“…Because G proteins are involved in the signaling cascades of more than a thousand different receptors, complex phenotypes in association with the G␤3 rs5443 alleles have been described, although not without controversy (for review, see Siffert, 2005). Variants in GNB3 have also been attributed to pharmacogenomic effects, particularly on adrenergic and serotonergic mechanisms (Hauner et al, 2003;Schü rks et al, 2007;Wilkie et al, 2007). With regard to ARs, intracoronary administration of the ␣ 2 -AR agonist azepexole was associated with increased vasoconstriction in carriers of the 825T allele compared with persons with the wild-type C variant (Table 5) (Baumgart et al, 1999).…”

Section: Pharmacogenomics Of Gpcr Ligands In Cardiovascular Medicinementioning

confidence: 99%

Pharmacogenomics of G Protein-Coupled Receptor Ligands in Cardiovascular Medicine

Rosskopf

Michel²

2008

Pharmacol Rev

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A splice site polymorphism in the G-protein β subunit influences antidepressant efficacy in depression

Abstract: These results suggest that inheritance of the GNB3C825T allele may significantly influence antidepressant response and emphasises the potential importance of polymorphisms in genes in signalling cascades activated by commonly prescribed antidepressants.

Cited by 74 publications

References 57 publications

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Consensus paper of the WFSBP Task Force on Genetics: Genetics, epigenetics and gene expression markers of major depressive disorder and antidepressant response

Pharmacogenetics of antidepressant response

Pharmacogenomics of G Protein-Coupled Receptor Ligands in Cardiovascular Medicine

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