Trial reportNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2008
Pharmacogenetic analysis of genes implicated in rodent models of antidepressant response: association of TREK1 and treatment resistance in the STAR(*)D study.
Trial report in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 103 citations in OpenAlex.
- Genetic correlate of cognitive training response in schizophrenia.Neuropharmacology · 2013Trial
- Pharmacogenetics studies in STAR*D: strengths, limitations, and results.Psychiatric services (Washington, D.C.) · 2009Trial
- Genetics and Neurobiology of Treatment-Resistant Depression-A Review.International journal of molecular sciences · 2025Review
- Potassium channels in depression: emerging roles and potential targets.Cell & bioscience · 2024Review
- Review
- Polymorphisms of COMT and CREB1 are associated with treatment-resistant depression in a Chinese Han population.Journal of neural transmission (Vienna, Austria : 1996) · 2022Article
- Inclusion of genetic variants in an ensemble of gradient boosting decision trees does not improve the prediction of citalopram treatment response.Scientific reports · 2021Article
- Ion Channel Dysfunction and Neuroinflammation in Migraine and Depression.Frontiers in pharmacology · 2021Review
- Contribution of Neuronal and Glial Two-Pore-Domain Potassium Channels in Health and Neurological Disorders.Neural plasticity · 2021Review
- KScientific reports · 2020Article
- Tandem pore TWIK-related potassium channels and neuroprotection.Neural regeneration research · 2019Review
- The Genetics of Treatment-Resistant Depression: A Critical Review and Future Perspectives.The international journal of neuropsychopharmacology · 2019Review
- Role of TREK-1 in Health and Disease, Focus on the Central Nervous System.Frontiers in pharmacology · 2019Review
- Imaging Genetics and Genomics in Psychiatry: A Critical Review of Progress and Potential.Biological psychiatry · 2017Review
- Review of Cohort Studies for Mood Disorders.Psychiatry investigation · 2016Review
- Proteasome system dysregulation and treatment resistance mechanisms in major depressive disorder.Translational psychiatry · 2015Article
- The Role of the Two-Pore Domain Potassium Channel TREK-1 in the Therapeutic Effects of Escitalopram in a Rat Model of Poststroke Depression.CNS neuroscience & therapeutics · 2015Article
- Targeting two-pore domain K(+) channels TREK-1 and TASK-3 for the treatment of depression: a new therapeutic concept.British journal of pharmacology · 2015Review
- Effects of fluoxetine on protein expression of potassium ion channels in the brain of chronic mild stress rats.Acta pharmaceutica Sinica. B · 2015Article
- Susceptibility loci for heroin and cocaine addiction in the serotonergic and adrenergic pathways in populations of different ancestry.Pharmacogenomics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Recent rodent models of antidepressant response implicate a novel set of genes in mechanisms of antidepressant action. The authors examined variants in four such genes (KCNK2 (TREK1), SLC18A2 (VMAT2), S100A10, and HDAC5) for association with remission in a large effectiveness trial of antidepressant treatments. Subjects were drawn from the Sequenced Treatment Alternatives to Relieve Depression (STAR(*)D) study, a multicenter, prospective, effectiveness trial in major depressive disorder (MDD). Outpatients with nonpsychotic MDD were initially treated with citalopram for up to 14 weeks; those who did not remit with citalopram were sequentially randomized to a series of next-step treatments, each for up to 12 weeks. Single-nucleotide polymorphisms in four genes were examined for association with remission, defined as a clinician-rated Quick Inventory of Depressive Symptomatology (QIDS-C(16)) score < or =5. Of 1554 participants for whom DNA was available, 565 (36%) reached remission with citalopram treatment. No association with any of the four genes was identified. However, among the 751 who entered next-step treatment, variants in KCNK2 were associated with treatment response (Bonferroni-corrected, gene-based empirical p<0.001). In follow-up analyses, KCNK2 was also associated with effects of similar magnitude for third-step treatment among those with unsatisfactory benefit to both citalopram and one next-step pharmacotherapy (n=225). These findings indicate that genetic variation in KCNK2 may identify individuals at risk for treatment resistance. More broadly, they indicate the utility of animal models in identifying genes for pharmacogenetic studies of antidepressant response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.