Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2011 Feb 16:2:6.
doi: 10.3389/fphar.2011.00006. eCollection 2011.

Pharmacogenetics of antidepressants

Affiliations

Pharmacogenetics of antidepressants

Concetta Crisafulli et al. Front Pharmacol. .

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.

Keywords: SNP; antidepressants; depression; gene; pharmacogenetics.

PubMed Disclaimer

References

    1. Acheson A., Conover J. C., Fandl J. P., DeChiara T. M., Russell M., Thadani A., Squinto S. P., Yancopoulos G. D., Lindsay R. M. (1995). A BDNF autocrine loop in adult sensory neurons prevents cell death. Nature 374, 450–45310.1038/374450a0 - DOI - PubMed
    1. Agid Y., Buzsaki G., Diamond D. M., Frackowiak R., Giedd J., Girault J. A., Grace A., Lambert J. J., Manji H., Mayberg H., Popoli M., Prochiantz A., Richter-Levin G., Somogyi P., Spedding M., Svenningsson P., Weinberger D. (2007). How can drug discovery for psychiatric disorders be improved? Nat. Rev. Drug. Discov. 6, 189–20110.1038/nrd2217 - DOI - PubMed
    1. Albert P. R., Lemonde S. (2004). 5-HT1A receptors, gene repression, and depression: guilt by association. Neuroscientist 10, 575–59310.1177/1073858404267382 - DOI - PubMed
    1. Anttila S., Kampman O., Illi A., Rontu R., Lehtimaki T., Leinonen E. (2007). Association between 5-HT2A, TPH1 and GNB3 genotypes and response to typical neuroleptics: a serotonergic approach. BMC Psychiatry 7, 22.10.1186/1471-244X-7-22 - DOI - PMC - PubMed
    1. Arias B., Catalan R., Gasto C., Gutierrez B., Fananas L. (2003). 5-HTTLPR polymorphism of the serotonin transporter gene predicts non-remission in major depression patients treated with citalopram in a 12-weeks follow up study. J. Clin. Psychopharmacol. 23, 563–56710.1097/01.jcp.0000095350.32154.73 - DOI - PubMed