ArticleMolecular psychiatry2022
Contribution of schizophrenia polygenic burden to longitudinal phenotypic variance in 22q11.2 deletion syndrome.
Article in Molecular psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Genome-wide tandem repeat expansions modify schizophrenia risk in the presence of a 22q11.2 deletion.Molecular psychiatry · 2026Article
- Potential for Genomics to Help Guide Preventive Strategies in Psychiatry.JAMA psychiatry · 2026Article
- Disorganized Inhibitory Dynamics in Hippocampal area CA1 of 22q11.2 Deletion Mutant Mice.bioRxiv : the preprint server for biology · 2026Article
- Article
- Genetic influences on antidepressant side effects: a CYP2C19 gene variation and polygenic risk study in the Estonian Biobank.European journal of human genetics : EJHG · 2025Article
- Polygenic and pharmacogenomic contributions to medication dosing: a real-world longitudinal biobank study.Journal of translational medicine · 2025Article
- Evaluation of 100 Dutch cases with 16p11.2 deletion and duplication syndromes; from clinical manifestations towards personalized treatment options.European journal of human genetics : EJHG · 2024Article
- Complex trait associations in rare diseases and impacts on Mendelian variant interpretation.Nature communications · 2024Article
- Multimorbidity in Severe Mental Illness as Part of the Neurodevelopmental Continuum: Physical Health-Related Endophenotypes of Schizophrenia-A Narrative Review.Brain sciences · 2024Review
- Complex trait associations in rare diseases and impacts on Mendelian variant interpretation.medRxiv : the preprint server for health sciences · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
While the recurrent 22q11.2 deletion is one of the strongest genetic risk factors for schizophrenia (SCZ), variability of its associated neuropsychiatric endophenotypes reflects its incomplete penetrance for psychosis development. To assess whether this phenotypic variability is linked to common variants associated with SCZ, we studied the association between SCZ polygenic risk score (PRS) and longitudinally acquired phenotypic information of the Swiss 22q11.2DS cohort (n = 97, 50% females, mean age 17.7 yr, mean visit interval 3.8 yr). The SCZ PRS with the best predictive performance was ascertained in the Estonian Biobank (n = 201,146) with LDpred. The infinitesimal SCZ PRS model showed the strongest capacity in discriminating SCZ cases from controls with one SD difference in SCZ PRS corresponding to an odds ratio (OR) of 1.73 (95% CI 1.57-1.90, P = 1.47 × 10
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