Evidence map›Paper›PMID 41074960›Full record

SynthesisPsychopharmacology2026

Integrating genome-wide and epigenome-wide associations for antipsychotic induced extrapyramidal side effects.

Kai Yao, Johan H Thygesen, Siobhan K Lock, Antonio F Pardiñas, Antonia L Pritchard, Israa Elbashir, Abdullah Lodhi, Zain-Ul-Abideen Ahmad, Michael C O'Donovan, Michael J Owen and 4 more

Abstract readMeta-Analysis
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Psychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Kai YaoMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK.
Johan H ThygesenInstitute of Health Informatics, University College London, 222 Euston Road, NW1 2DA, London, UK.
Siobhan K LockCentre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Hadyn Ellis Building, Cardiff, CF24 4HQ, Cardiff, UK.
Antonio F PardiñasCentre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Hadyn Ellis Building, Cardiff, CF24 4HQ, Cardiff, UK.
Antonia L PritchardDivision of Biomedical Science, University of the Highlands and Islands, An Lochran, Inverness, IV2 5NA, UK.
Israa ElbashirMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK.
Abdullah LodhiMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK.
Zain-Ul-Abideen AhmadMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK.
Michael C O'DonovanCentre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Hadyn Ellis Building, Cardiff, CF24 4HQ, Cardiff, UK.
Michael J OwenCentre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Hadyn Ellis Building, Cardiff, CF24 4HQ, Cardiff, UK.
James T R WaltersCentre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Hadyn Ellis Building, Cardiff, CF24 4HQ, Cardiff, UK.
David St ClairSchool of Medicine, Medical Sciences, Nutrition University of Aberdeen, King's College, Aberdeen, AB24 3FX, UK.
Nick BassMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK.
Andrew McQuillinMolecular Psychiatry Laboratory, Division of Psychiatry, University College London, Rockefeller Building, 21 University Street, London, WC1E 6BT, UK. a.mcquillin@ucl.ac.uk.ORCID http://orcid.org/0000-0003-1567-2240

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleAntipsychotic medications are the first-line treatment for schizophrenia. Around 40% of people who are treated with antipsychotics could develop extrapyramidal side-effects (EPSE) including: (1) Dyskinesia, (2) Parkinsonism, (3) Akathisia, and (4) Dystonia.

objectivesThis study aimed to identify genetic risk factors for EPSE presence following antipsychotic treatment.

methodsWe conducted Genome-wide association (GWAS) and Epigenome-wide association (EWAS) meta-analyses of EPSE, with subset analyses separating first and second generation antipsychotic (FGA/SGA) exposure. We integrated significant EWAS findings from a between-case design to a comparable GWAS for association enrichment. We investigated whether polygenic risk scores (PRS) for schizophrenia, Parkinson's disease, and Lewy-body dementia could predict EPSE.

resultsThe primary GWAS top SNP rs2709733 (A/G) (p = 5.755 × 10

conclusionsOur study sheds new light on the potential biological mechanisms underlying EPSE development in schizophrenia, highlighting the importance of exploring both methylation changes and SNP associations.

Indexed as

Antipsychotic AgentsBasal Ganglia DiseasesEpigenomeGenetic Risk ScoreGenome-Wide Association StudyHumansPolymorphism, Single NucleotideSchizophreniaAntipsychotic AgentsAntipsychoticEpigenome-wide associationExtrapyramidal side-effectsGenome-wide associationSchizophrenia

Identifiers

PMID41074960
PMCPMC13433426

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Registered trials

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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.