Serotonin Transporter Polymorphisms and Side Effects in Antidepressant Therapy – A Pilot Study

Popp, Johannes; Leucht, Stefan; Heres, Stephan; Steimer, Werner

doi:10.2217/14622416.7.2.159

Cited by 59 publications

(31 citation statements)

References 21 publications

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“…Single-photon emission computed tomography and positron emission tomography (PET) studies reported that higher pre-treatment availability and greater SSRI occupancy of the SERT might predict better treatment response (Kugaya et al 2004;Yeh et al 2015). The most confirmed pharmacogenetic finding was an association of the S allele with worse antidepressant efficacy than the LL genotype in Caucasian patients treated with SSRIs (Porcelli et al 2012). Relatively fewer studies genotyped the triallelic locus and they did not support a substantial role of the polymorphism on antidepressant efficacy (Fabbri et al 2013a).…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

“…Relatively fewer studies genotyped the triallelic locus and they did not support a substantial role of the polymorphism on antidepressant efficacy (Fabbri et al 2013a). Several pharmacogenetic studies (Perlis et al 2003;Murphy et al 2004;Popp et al 2006;Hu et al 2007;Smits et al 2007;Maron et al 2009) and one meta-analysis (Kato and Serretti 2010) reported that the S allele may also be a risk factor for the development of SSRI-induced side effects in Caucasian populations, though not for sexual dysfunction (Bishop et al 2009;Strohmaier et al 2011).…”

Section: Genetic Polymorphismsmentioning

confidence: 99%

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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: Genetic Polymorphismsmentioning

confidence: 99%

Section: Genetic Polymorphismsmentioning

confidence: 99%

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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show abstract

“…204 Some studies were not able to replicate these findings. 83,205 The Stin2 10/12 allele has also been found to be associated with greater side effects, 206 but lack of association with side effects has also been reported. 163 More recently, an SNP (rs25531) located just upstream of 5-HTTLPR was reported to affect antidepressant response, and it was shown to modulate the effect of other 5-HTTLPR alleles.…”

Section: Comtmentioning

confidence: 99%

Pharmacogenetics of antidepressant response

Porcelli

Drago

Fabbri

et al. 2011

J Psychiatry Neurosci

160

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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“…Remission was defined as a final score of 7 or less on the Hamilton Depression Rating Scale (HAM-D), while a response was defined to be a decrease of at least 50% in the total score on the HAM-D or [20][21][22][23][24][28][29][30][31][32]35,36,37,54,[56][57][58][59][60][61][62][63][64][65][66][67][68][69] [19,25,26,33,70,71] STin2 [28,29,56] [ 26,29,57,71,72] Dopamine transpoter Dopamine transporter VNTR [61] Norepinephrine transporter Norepinephrine transporter G1287A [26,29] -T-182C - [26] Serotonin receptor 5-HT1A Serotonin autoreceptor C(-1019)G [57,[73][74]…”

Section: Results N Literature Searchmentioning

confidence: 99%

Application of Pharmacogenomics to Clinical Problems in Depression

Oestergaard

Møldrup

2009

Personalized Medicine

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The goal of this article is to review the literature for evidence supporting an association between polymorphisms within drug target genes and clinical outcomes for treating depression, with a purpose to identify a research area having the most promising potential to be introduced into clinical settings, and thus, discussing the perspectives of genotyping in antidepressant therapy. A total of 67 articles were identified. Polymorphic sites within the serotonin transporter gene promoter, 5-HTTLPR, were the most studied polymorphisms. All except three articles were designed as cohort studies. The other three articles included two meta-analyses and one decision-analytic model. The main finding from these meta-analyses was that the l variant was associated with a better response to selective serotonin reuptake inhibitors. The main conclusion from the decision-analytic model study was that performing genetic testing before prescribing antidepressant treatment may lead to greater numbers of patients experiencing remission early in treatment. Clinical outcomes of genotyping this polymorphism were evaluated by improvement of depression score, odds ratio and absolute risk reduction.

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Serotonin Transporter Polymorphisms and Side Effects in Antidepressant Therapy – A Pilot Study

Cited by 59 publications

References 21 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

Application of Pharmacogenomics to Clinical Problems in Depression

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