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Genetic and epigenetic predictors of antidepressant response
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DOI：10.1016/j.pnpbp.2026.111738.png)
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Abstract
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• Major depressive disorder is a major global burden, and fewer than a third remit after a first-line medication trial. • Genetic and epigenetic variability supports personalised approaches to antidepressant response. • Candidate gene variants (e.g. SLC6A4, HTR2A, BDNF) show small and inconsistent effects, limiting clinical utility. • CYP2D6, CYP2C19 and CYP2B6 genotypes inform drug metabolism and dosing better than efficacy prediction. • Genome-wide studies show antidepressant response is highly polygenic, with no robust loci ready for clinical use. • Polygenic risk scores show modest predictive ability but are not yet ready for routine clinical implementation. • DNA methylation and non-coding RNA markers are promising but lack replication and standardisation. • Transcriptomic and inflammatory signatures may help stratify patients, though findings remain preliminary. • Panel-based pharmacogenetic testing offers modest clinical benefits, mainly by guiding dosing and tolerability. • Multi-omics approaches are promising but remain investigational and require larger, more diverse cohorts. • Clinical translation requires larger, harmonised, medication-aware cohorts with greater ancestry diversity. • Precision antidepressant prescribing remains a goal beyond pharmacokinetic dosing guidance.
Keywords:
antidepressant response
pharmacogenetics
polygenic risk scores
DNA methylation
precision medicine
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