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BibTeX
Genome-wide association study reveals greater polygenic loading for schizophrenia in cases with a family history of illness
American journal of medical genetics. Part B, Neuropsychiatric genetics, 2016-03, Vol.171B (2), p.276-289
Bigdeli, Tim B.
Ripke, Stephan
Bacanu, Silviu-Alin
Lee, Sang Hong
Wray, Naomi R.
Gejman, Pablo V.
Rietschel, Marcella
Cichon, Sven
St Clair, David
Corvin, Aiden
Kirov, George
McQuillin, Andrew
Gurling, Hugh
Rujescu, Dan
Andreassen, Ole A.
Werge, Thomas
Blackwood, Douglas H. R.
Pato, Carlos N.
Pato, Michele T.
Malhotra, Anil K.
O'Donovan, Michael C.
Kendler, Kenneth S.
Fanous, Ayman H.
2016
Details
Autor(en) / Beteiligte
Bigdeli, Tim B.
Ripke, Stephan
Bacanu, Silviu-Alin
Lee, Sang Hong
Wray, Naomi R.
Gejman, Pablo V.
Rietschel, Marcella
Cichon, Sven
St Clair, David
Corvin, Aiden
Kirov, George
McQuillin, Andrew
Gurling, Hugh
Rujescu, Dan
Andreassen, Ole A.
Werge, Thomas
Blackwood, Douglas H. R.
Pato, Carlos N.
Pato, Michele T.
Malhotra, Anil K.
O'Donovan, Michael C.
Kendler, Kenneth S.
Fanous, Ayman H.
Titel
Genome-wide association study reveals greater polygenic loading for schizophrenia in cases with a family history of illness
Ist Teil von
American journal of medical genetics. Part B, Neuropsychiatric genetics, 2016-03, Vol.171B (2), p.276-289
Ort / Verlag
United States: Blackwell Publishing Ltd
Erscheinungsjahr
2016
Link zum Volltext
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
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 R2 = 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. © 2015 Wiley Periodicals, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 1552-4841, 1552-485X
eISSN: 1552-485X
DOI: 10.1002/ajmg.b.32402
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5816590
Format
–
Schlagworte
Bipolar Disorder - genetics
,
Case-Control Studies
,
Depressive Disorder, Major - genetics
,
Family
,
family history
,
Genetic Predisposition to Disease
,
Genome-Wide Association Study
,
GWAS
,
Humans
,
Inheritance Patterns - genetics
,
Medicin och hälsovetenskap
,
Models, Genetic
,
Multifactorial Inheritance - genetics
,
polygenic
,
Polymorphism, Single Nucleotide - genetics
,
schizophrenia
,
Schizophrenia - genetics
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