Pharmacogenetics of antidepressants

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Standard

Pharmacogenetics of antidepressants. / Crisafulli, Concetta; Fabbri, Chiara; Porcelli, Stefano; Drago, Antonio; Spina, Edoardo; De Ronchi, Diana; Serretti, Alessandro.

I: Frontiers in Pharmacology, Bind 2, Nr. 6, 2011.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avisTidsskriftartikelForskningpeer review

Harvard

Crisafulli, C, Fabbri, C, Porcelli, S, Drago, A, Spina, E, De Ronchi, D & Serretti, A 2011, 'Pharmacogenetics of antidepressants', Frontiers in Pharmacology, bind 2, nr. 6. https://doi.org/10.3389/fphar.2011.00006

APA

Crisafulli, C., Fabbri, C., Porcelli, S., Drago, A., Spina, E., De Ronchi, D., & Serretti, A. (2011). Pharmacogenetics of antidepressants. Frontiers in Pharmacology, 2(6). https://doi.org/10.3389/fphar.2011.00006

CBE

Crisafulli C, Fabbri C, Porcelli S, Drago A, Spina E, De Ronchi D, Serretti A. 2011. Pharmacogenetics of antidepressants. Frontiers in Pharmacology. 2(6). https://doi.org/10.3389/fphar.2011.00006

MLA

Crisafulli, Concetta o.a.. "Pharmacogenetics of antidepressants". Frontiers in Pharmacology. 2011. 2(6). https://doi.org/10.3389/fphar.2011.00006

Vancouver

Crisafulli C, Fabbri C, Porcelli S, Drago A, Spina E, De Ronchi D o.a. Pharmacogenetics of antidepressants. Frontiers in Pharmacology. 2011;2(6). https://doi.org/10.3389/fphar.2011.00006

Author

Crisafulli, Concetta ; Fabbri, Chiara ; Porcelli, Stefano ; Drago, Antonio ; Spina, Edoardo ; De Ronchi, Diana ; Serretti, Alessandro. / Pharmacogenetics of antidepressants. I: Frontiers in Pharmacology. 2011 ; Bind 2, Nr. 6.

Bibtex

@article{c564dd2acfaa483389c2b2d8192107d1,
title = "Pharmacogenetics of antidepressants",
abstract = "Up to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects.",
author = "Concetta Crisafulli and Chiara Fabbri and Stefano Porcelli and Antonio Drago and Edoardo Spina and {De Ronchi}, Diana and Alessandro Serretti",
year = "2011",
doi = "10.3389/fphar.2011.00006",
language = "English",
volume = "2",
journal = "Frontiers in Pharmacology",
issn = "1663-9812",
publisher = "Frontiers Research Foundation",
number = "6",

}

RIS

TY - JOUR

T1 - Pharmacogenetics of antidepressants

AU - Crisafulli, Concetta

AU - Fabbri, Chiara

AU - Porcelli, Stefano

AU - Drago, Antonio

AU - Spina, Edoardo

AU - De Ronchi, Diana

AU - Serretti, Alessandro

PY - 2011

Y1 - 2011

N2 - Up to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects.

AB - Up to 60% of depressed patients do not respond completely to antidepressants (ADs) and up to 30% do not respond at all. Genetic factors contribute for about 50% of the AD response. During the recent years the possible influence of a set of candidate genes as genetic predictors of AD response efficacy was investigated by us and others. They include the cytochrome P450 superfamily, the P-glycoprotein (ABCB1), the tryptophan hydroxylase, the catechol-O-methyltransferase, the monoamine oxidase A, the serotonin transporter (5-HTTLPR), the norepinephrine transporter, the dopamine transporter, variants in the 5-hydroxytryptamine receptors (5-HT1A, 5-HT2A, 5-HT3A, 5-HT3B, and 5-HT6), adrenoreceptor beta-1 and alpha-2, the dopamine receptors (D2), the G protein beta 3 subunit, the corticotropin releasing hormone receptors (CRHR1 and CRHR2), the glucocorticoid receptors, the c-AMP response-element binding, and the brain-derived neurotrophic factor. Marginal associations were reported for angiotensin I converting enzyme, circadian locomotor output cycles kaput protein, glutamatergic system, nitric oxide synthase, and interleukin 1-beta gene. In conclusion, gene variants seem to influence human behavior, liability to disorders and treatment response. Nonetheless, gene × environment interactions have been hypothesized to modulate several of these effects.

U2 - 10.3389/fphar.2011.00006

DO - 10.3389/fphar.2011.00006

M3 - Journal article

C2 - 21687501

VL - 2

JO - Frontiers in Pharmacology

JF - Frontiers in Pharmacology

SN - 1663-9812

IS - 6

ER -