ArticleTranslational psychiatry2018
Genetic risk for schizophrenia and autism, social impairment and developmental pathways to psychosis.
Article in Translational psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- The IMAGEN study: a decade of imaging genetics in adolescents.Molecular psychiatry · 2020Pooled it
- The reporting and handling of missing data in genetic epidemiological studies of mental health in childhood and adolescence: A systematic review.JCPP advances · 2026Article
- Unraveling the Shared Genetic Architecture and Polygenic Overlap Between Loneliness, Major Depressive Disorder, and Sleep-Related Traits.Biomedicines · 2025Article
- Schizotypy, Psychosis Proneness, and the Polygenic Risk for Schizophrenia and Resilience.Schizophrenia bulletin · 2025Article
- Association of Polygenic Risk Scores for Schizophrenia with Psychosis-Proneness Indicators in the General Population: A Narrative Review.Consortium psychiatricum · 2025Review
- Validation of the Hebrew version of the Community Assessment of Psychic Experiences in a sample of Israeli Hebrew speakers.Frontiers in psychiatry · 2025Article
- Polygenic risk of social isolation behavior and its influence on psychopathology and personality.Molecular psychiatry · 2024Article
- Schizophrenia polygenic risk score in psychosis proneness.European archives of psychiatry and clinical neuroscience · 2023Article
- Patterns of brain asymmetry associated with polygenic risks for autism and schizophrenia implicate language and executive functions but not brain masculinization.Molecular psychiatry · 2021Article
- Autistic traits in psychotic disorders: prevalence, familial risk, and impact on social functioning.Psychological medicine · 2021Article
- Why Psychotropic Drugs Don't Cure Mental Illness-But Should They?Frontiers in psychiatry · 2021Article
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- Validity of polygenic risk scores: are we measuring what we think we are?Human molecular genetics · 2019Review
- Treatment-Resistant Schizophrenia: Insights From Genetic Studies and Machine Learning Approaches.Frontiers in pharmacology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
32 authors at 20 institutions in 9 countries.
Funding
Abstract
While psychotic experiences (PEs) are assumed to represent psychosis liability, general population studies have not been able to establish significant associations between polygenic risk scores (PRS) and PEs. Previous work suggests that PEs may only represent significant risk when accompanied by social impairment. Leveraging data from the large longitudinal IMAGEN cohort, including 2096 14-year old adolescents that were followed-up to age 18, we tested whether the association between polygenic risk and PEs is mediated by (increasing) impairments in social functioning and social cognitive processes. Using structural equation modeling (SEM) for the subset of participants (n = 643) with complete baseline and follow-up data, we examined pathways to PEs. We found that high polygenic risk for schizophrenia (p = 0.014), reduced brain activity to emotional stimuli (p = 0.009) and social impairments in late adolescence (p < 0.001; controlling for functioning in early adolescence) each independently contributed to the severity of PEs at age 18. The pathway between polygenic risk for autism spectrum disorder and PEs was mediated by social impairments in late adolescence (indirect pathway; p = 0.025). These findings point to multiple direct and indirect pathways to PEs, suggesting that different processes are in play, depending on genetic loading, and environment. Our results suggest that treatments targeting prevention of social impairment may be particularly promising for individuals at genetic risk for autism in order to minimize risk for psychosis.
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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.