ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2016
Genome-wide association study reveals greater polygenic loading for schizophrenia in cases with a family history of illness.
Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Demographic, Premorbid, and Clinical Characteristics of Schizophrenia Spectrum Patients with High and Low Polygenic Liability to the Disorder.Diseases (Basel, Switzerland) · 2025Article
- Why mismatch negativity continues to hold potential in probing altered brain function in schizophrenia.PCN reports : psychiatry and clinical neurosciences · 2023Review
- Postictal Psychosis in Epilepsy: A Clinicogenetic Study.Annals of neurology · 2021Article
- Mood-Stabilizing Antiepileptic Treatment Response in Bipolar Disorder: A Genome-Wide Association Study.Clinical pharmacology and therapeutics · 2020Article
- Label-free proteomics differences in the dorsolateral prefrontal cortex between bipolar disorder patients with and without psychosis.Journal of affective disorders · 2020Article
- Familial and socioeconomic contributions to premorbid functioning in psychosis: Impact on age at onset and treatment response.European psychiatry : the journal of the Association of European Psychiatrists · 2020Article
- The abiding relevance of mouse models of rare mutations to psychiatric neuroscience and therapeutics.Schizophrenia research · 2020Article
- Evaluating the Impact of Nonrandom Mating: Psychiatric Outcomes Among the Offspring of Pairs Diagnosed With Schizophrenia and Bipolar Disorder.Biological psychiatry · 2020Article
- Characteristics of youth with reported family history of psychosis spectrum symptoms in the Philadelphia Neurodevelopmental Cohort.Schizophrenia research · 2020Article
- Candidate CSPG4 mutations and induced pluripotent stem cell modeling implicate oligodendrocyte progenitor cell dysfunction in familial schizophrenia.Molecular psychiatry · 2019Article
- Polygenic risk scores in psychiatry: Will they be useful for clinicians?F1000Research · 2019Review
- Use of schizophrenia and bipolar disorder polygenic risk scores to identify psychotic disorders.The British journal of psychiatry : the journal of mental science · 2018Article
- Genetic risk scores and family history as predictors of schizophrenia in Nordic registers.Psychological medicine · 2018Article
- Consanguineous Marriage and the Psychopathology of Progeny: A Population-wide Data Linkage Study.JAMA psychiatry · 2018Observational
- Statistical methods to detect pleiotropy in human complex traits.Open biology · 2017Review
- Impact of Familial Loading on Prefrontal Activation in Major Psychiatric Disorders: A Near-Infrared Spectroscopy (NIRS) Study.Scientific reports · 2017Article
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24 authors.
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Abstract
Genome-wide association studies (GWAS) of schizophrenia have yielded more than 100 common susceptibility variants, and strongly support a substantial polygenic contribution of a large number of small allelic effects. It has been hypothesized that familial schizophrenia is largely a consequence of inherited rather than environmental factors. We investigated the extent to which familiality of schizophrenia is associated with enrichment for common risk variants detectable in a large GWAS. We analyzed single nucleotide polymorphism (SNP) data for cases reporting a family history of psychotic illness (N = 978), cases reporting no such family history (N = 4,503), and unscreened controls (N = 8,285) from the Psychiatric Genomics Consortium (PGC1) study of schizophrenia. We used a multinomial logistic regression approach with model-fitting to detect allelic effects specific to either family history subgroup. We also considered a polygenic model, in which we tested whether family history positive subjects carried more schizophrenia risk alleles than family history negative subjects, on average. Several individual SNPs attained suggestive but not genome-wide significant association with either family history subgroup. Comparison of genome-wide polygenic risk scores based on GWAS summary statistics indicated a significant enrichment for SNP effects among family history positive compared to family history negative cases (Nagelkerke's R(2 ) = 0.0021; P = 0.00331; P-value threshold <0.4). Estimates of variability in disease liability attributable to the aggregate effect of genome-wide SNPs were significantly greater for family history positive compared to family history negative cases (0.32 and 0.22, respectively; P = 0.031). We found suggestive evidence of allelic effects detectable in large GWAS of schizophrenia that might be specific to particular family history subgroups. However, consideration of a polygenic risk score indicated a significant enrichment among family history positive cases for common allelic effects. Familial illness might, therefore, represent a more heritable form of schizophrenia, as suggested by previous epidemiological studies.
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