Pharmacogenetics of antidepressants

Concetta Crisafulli, Chiara Fabbri, Stefano Porcelli, Antonio Drago, Edoardo Spina, Diana De Ronchi, Alessandro Serretti

Research output: Contribution to journalArticlepeer-review

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-Omethyltransferase, 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.

Original languageEnglish
Article numberArticle 6
JournalFrontiers in Pharmacology
VolumeFEB
DOIs
Publication statusPublished - 2011

Keywords

  • Antidepressants
  • Depression
  • Gene
  • Pharmacogenetics
  • Snp

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology

Fingerprint Dive into the research topics of 'Pharmacogenetics of antidepressants'. Together they form a unique fingerprint.

Cite this