ArticleTranslational psychiatry2018
Exploratory genome-wide association analysis of response to ketamine and a polygenic analysis of response to scopolamine in depression.
Article in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers, 1 of them a synthesis that pooled it.
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
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Pharmacogenomic scores in psychiatry: systematic review of current evidence.Translational psychiatry · 2024Pooled it
- Genetics of Response to ECT, TMS, Ketamine and Esketamine.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2025Review
- Personalized use of ketamine and esketamine for treatment-resistant depression.Translational psychiatry · 2024Review
- Pharmacogenomics polygenic risk score: Ready or not for prime time?Clinical and translational science · 2024Review
- Applying polygenic risk score methods to pharmacogenomics GWAS: challenges and opportunities.Briefings in bioinformatics · 2023Article
- Article
- Genome-Wide Association Study on Three Behaviors Tested in an Open Field in Heterogeneous Stock Rats Identifies Multiple Loci Implicated in Psychiatric Disorders.Frontiers in psychiatry · 2022Article
- Molecular Mechanisms Associated with Antidepressant Treatment on Major Depression.Complex psychiatry · 2021Review
- Experimental Therapeutics in Treatment-Resistant Major Depressive Disorder.Journal of experimental pharmacology · 2021Review
- Rodent models of post-traumatic stress disorder: behavioral assessment.Translational psychiatry · 2020Review
- Genetic Intersections of Language and Neuropsychiatric Conditions.Current psychiatry reports · 2020Review
- Delineating significant genome-wide associations of variants with antipsychotic and antidepressant treatment response: implications for clinical pharmacogenomics.Human genomics · 2020Article
- Neurobiological biomarkers of response to ketamine.Advances in pharmacology (San Diego, Calif.) · 2020Review
- Translating Molecular and Neuroendocrine Findings in Posttraumatic Stress Disorder and Resilience to Novel Therapies.Biological psychiatry · 2019Review
- Pharmacogenetics and Depression: A Critical Perspective.Psychiatry investigation · 2019Article
- Biomarkers of ketamine's antidepressant effect: a clinical review of genetics, functional connectivity, and neurophysiology.Chronic stress (Thousand Oaks, Calif.)Review
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 8 institutions in 1 country.
Funding
Abstract
Growing evidence suggests that the glutamatergic modulator ketamine has rapid antidepressant effects in treatment-resistant depressed subjects. The anticholinergic agent scopolamine has also shown promise as a rapid-acting antidepressant. This study applied genome-wide markers to investigate the role of genetic variants in predicting acute antidepressant response to both agents. The ketamine-treated sample included 157 unrelated European subjects with major depressive disorder (MDD) or bipolar disorder (BD). The scopolamine-treated sample comprised 37 unrelated European subjects diagnosed with either MDD or BD who had a current Major Depressive Episode (MDE), and had failed at least two adequate treatment trials for depression. Change in Montgomery-Asberg Depression Rating Scale (MADRS) or the 17-item Hamilton Depression Rating Scale (HAM-D) scale scores at day 1 (24 h post-treatment) was considered the primary outcome. Here, we conduct pilot genome-wide association study (GWAS) analyses to identify potential markers of ketamine response and dissociative side effects. Polygenic risk score analysis of SNPs ranked by the strength of their association with ketamine response was then calculated in order to assess whether common genetic markers from the ketamine study could predict response to scopolamine. Findings require replication in larger samples in light of low power of analyses of these small samples. Neverthless, these data provide a promising illustration of our future potential to identify genetic variants underlying rapid treatment response in mood disorders and may ultimately guide individual patient treatment selection in the future.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.