Genetics and Personalized Medicine in Antidepressant Treatment

Gvozdic, Katarina; Brandl, Eva J.; Taylor, Danielle L.; Müller, Daniel J.

doi:10.2174/138161212803523617

Cited by 21 publications

(5 citation statements)

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“…There is currently no strong evidence supporting gene‐based dosing recommendations for other cytochrome P450 enzymes that metabolize SSRIs. There is increasing evidence that variations in the genes encoding the serotonin transporter (5‐HTT, SLC6A4) and the serotonin 2A receptor (HTR2A) are associated with SSRI response and adverse effects . As additional studies are published, gene‐based dosing recommendations for SLC6A4 and/or HTR2A may be warranted.…”

Section: Drugs: Ssrismentioning

confidence: 99%

Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors

Hicks

Bishop

Sangkuhl

et al. 2015

Clin Pharma and Therapeutics

815

791

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Selective Serotonin Reuptake Inhibitors (SSRIs) are primary treatment options for major depressive and anxiety disorders. CYP2D6 and CYP2C19 polymorphisms can influence the metabolism of SSRIs thereby affecting drug efficacy and safety. We summarize evidence from the published literature supporting these associations and provide dosing recommendations for fluvoxamine, paroxetine, citalopram, escitalopram and sertraline based on CYP2D6 and/or CYP2C19 genotype (updates at www.pharmgkb.org).

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Section: Drugs: Ssrismentioning

confidence: 99%

Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors

Hicks

Bishop

Sangkuhl

et al. 2015

Clin Pharma and Therapeutics

815

791

View full text Add to dashboard Cite

show abstract

“…In MDD, significant work has been done in this area and has implicated polymorphisms in a number of genes as predictors of antidepressant response [74, 75]. In contrast, progress in establishing genetic polymorphisms with predictive value in OCD has been relatively slow [76].…”

Section: Pharmacogeneticsmentioning

confidence: 99%

Pharmacological Treatment of Obsessive-Compulsive Disorder

Pittenger

Bloch

2014

Psychiatric Clinics of North America

144

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Synopsis Obsessive-compulsive disorder (OCD) affects up to 2.5% of the population of the course of a lifetime and produces substantial morbidity. Approximately 70% of patients can experience significant symptomatic relief with appropriate pharmacotherapy. The selective serotonin reuptake inhibitors (SSRIs) are the main stay of pharmacological treatment. These are typically used at higher doses and for longer periods than in depression. Remission is, unfortunately, uncommon. Proven second-line treatments include the tricyclic clomipramine and the addition of low-dose neuroleptic medications. Other augmentation strategies have been explored for patients refractory to proven interventions, but they are not as of yet robustly supported by controlled studies. The combination of medication with psychotherapy is often used, though careful studies have not documented synergistic benefit in adult patients. OCD refractory to available treatments remains a profound clinical challenge.

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“…These studies pertain to epigenetic mechanisms underlying p11 involvement in AD interventions. Using the PubMed database of publications to mid 2011, Gvozdic et al [218] reviewed the available literature on pharmacogenetics of AD response and side effects. They observed that several variants in candidate genes involved in the pharmacokinetics or pharmacodynamics of ADs, including association findings in the serotonin transporter gene 5-HTT , serotonin receptor genes, a gene coding an efflux pump in the blood-brain-barrier ( ABCB1 ), and genes involved in the HPA axis.…”

Section: Pharmacogenetics Of Mood Disorder Treatmentmentioning

confidence: 99%

Epigenetic Modulation of Mood Disorders

Archer

Blum²,

Ms³

2013

J Genet Syndr Gene Ther

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Background Mood disorders are expressed in many heterogeneous forms, varying from anxiety to severe major clinical depression. The disorders are expressed in individual variety through manifestations governed by co-morbidities, symptom frequency, severity, and duration, and the effects of genes on phenotypes. The underlying etiologies of mood disorders consist of complex interactive operations of genetic and environmental factors. The notion of endophenotypes, which encompasses the markers of several underlying liabilities to the disorders, may facilitate efforts to detect and define, through staging, the genetic risks inherent to the extreme complexity of disease state. Aims This review evaluates the role of genetic biomarkers in assisting clinical diagnosis, identification of risk factors, and treatment of mood disorders. Methods Through a systematic assessment of studies investigating the epigenetic basis for mood disorders, the present review examines the interaction of genes and environment underlying the pathophysiology of these disorders. Results The majority of research findings suggest that the notion of endophenotypes, which encompasses the markers of several underlying liabilities to the disorders, may facilitate efforts to detect and define, through staging, the genetic risks inherent to the extreme complexity of the disease states. Several strategies under development and refinement show the propensity for derivation of essential elements in the etiopathogenesis of the disorders affecting drug-efficacy, drug metabolism, and drug adverse effects, e.g., with regard to selective serotonin reuptake inhibitors. These include: transporter gene expression and genes encoding receptor systems, hypothalamic-pituitary-adrenal axis factors, neurotrophic factors, and inflammatory factors affecting neuroimmune function. Nevertheless, procedural considerations of pharmacogenetics presume the parallel investment of policies and regulations to withstand eventual attempts at misuse, thereby ensuring patient integrity. Conclusions Identification of genetic biomarkers facilitates choice of treatment, prediction of response, and prognosis of outcome over a wide spectrum of symptoms associated with affective states, thereby optimizing clinical practice procedures. Epigenetic regulation of primary brain signaling, e.g., serotonin and hypothalamic-pituitary-adrenal function, and factors governing their metabolism are necessary considerations. The participation of neurotrophic factors remains indispensable for neurogenesis, survival, and functional maintenance of brain systems.

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Genetics and Personalized Medicine in Antidepressant Treatment

Cited by 21 publications

References 0 publications

Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors

Clinical Pharmacogenetics Implementation Consortium (CPIC) Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Selective Serotonin Reuptake Inhibitors

Pharmacological Treatment of Obsessive-Compulsive Disorder

Epigenetic Modulation of Mood Disorders

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