Pharmacogenetics Studies in STAR*D: Strengths, Limitations, and Results
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Several lines of evidence support an important genetic contribution to the wide individual variation in therapeutic response to antidepressant medications. The Sequenced Treatment Alternatives to Relieve Depression (STAR*D) study provided the largest cohort assembled to date of DNA from patients with nonpsychotic major depressive disorder, uniformly treated with citalopram and followed prospectively for up to 12 weeks. This pivotal study changed the face of pharmacogenetics research by increasing the sample size by an order of magnitude as well as by providing detailed prospective information about antidepressant response and tolerability. Several groups have identified markers in genes and tested the replication of previous findings of genes associated with outcome and side effects of antidepressant treatment. Variants in HTR2A, GRIK4, and KCNK2 were associated with citalopram treatment outcome. Replication was achieved in markers in the FKBP5 gene. Other findings in PDE11A and BDNF were not successfully replicated, and reports of potential confounders in previous associations with serotonin transporter variation (SLC6A4) were identified. Polymorphisms in pharmacokinetic genes involved in metabolism and transmembrane transport were also not associated with antidepressant response. Adverse events were also tested. Treatment-emergent suicidal ideation was associated with GRIK2, GRIA3, PAPLN, IL28RA, and CREB1. Sexual dysfunction was linked with variation in GRIN3A, GRIA1 GRIA3, and GRIK2. Reported and future findings of pharmacogenetics studies in STAR*D could help elucidate pathways involved in major depression and those pertinent to antidepressant outcome and side effects. Replication of these findings in independent samples could lead to the development of new treatments and to optimization of available treatments.
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FKBP51 gene variants are associated with antidepressant response, depression disease status, suicide, personality traits, recovery from psychosocial stress, peritraumatic dissociation, PTSD, and modify effects of early life trauma in PTSD and major depression.
“This study was the first to identify a correlation of FKBP51 gene variants with response to antidepressant treatment, and also with the reactivity of the HPA axis in the dexamethasone (DEX)-CRH test.”
From FKBP51 and FKBP52 in signaling and disease (2011) · cites this paper as [59]
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- Authors
- Laje, G., Perlis, R. H., Rush, A. J., & McMahon, F. J.
- Affiliations
- National Institute of Mental Health (US)
- Harvard University (US)
- National University of Singapore (SG)
- Venue
- Psychiatric Services
- Published
- 2009-11
- Volume
- 60
- Issue
- 11
- Pages
- 1446-1457
- ISSN
- 0022-1597 (ISSN-L)
- 1075-2730
- 1557-9700
- PMC
- PMC3775610
- OpenAlex
- W2121016639
- Cited by
- 89
- References
- 66
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 5 · 2015: 3 · 2014: 8 · 2013: 9 · 2012: 7
- FWCI
- 9.14
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychiatric Services (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- National University of Singapore (submittedVersion)
- Funders
- U.S. Department of Health and Human Services
- Bristol-Myers Squibb
- Eli Lilly and Company
- Pfizer
- AstraZeneca
- GlaxoSmithKline
- National Institutes of Health (n01mh90003-26-0-0, N01MH90003)
- National Institute of Mental Health (N01‐MH‐90003, MH90003, N01 MH090003, K23MH067060, K23-MH67060)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Pharmacogenetics and Drug Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- pharmacogenetics, major depressive disorder, antidepressant response, citalopram, antidepressant side effects, sexual dysfunction, HTR2A, GRIK4, KCNK2, FKBP5, brain-derived neurotrophic factor, PDE11A, serotonin transporter, pharmacokinetic genes, genetic polymorphism, replication
- MeSH terms
- Venlafaxine Hydrochloride, Adult, Buspirone, Cyclohexanols, Depressive Disorder, Major, Major Depressive Disorder, Humans, Pharmacogenetics, Phenotype, Citalopram, Biomarkers, Comorbidity, Cognitive Behavioral Therapy, Bupropion, Treatment Outcome, Treatment Failure, Serotonin Receptor Agonists, Selective Serotonin Reuptake Inhibitors, Receptors, Kainic Acid, Kainic Acid Receptors, Dopamine Uptake Inhibitors, Sertraline, Polymorphism, Single Nucleotide, Receptor, Serotonin, 5-HT2A, Serotonin Plasma Membrane Transport Proteins
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