| Autor: |
Szatkiewicz J; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA., Crowley JJ; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA., Adolfsson AN; Department of Clinical Sciences and Psychiatry, University of Umeå, Umeå, Sweden., Åberg KA; Center for Biomarker Research and Precision Medicine, Virginia Commonwealth University, Richmond, VA, USA., Alaerts M; Center of Medical Genetics, University of Antwerp and Antwerp University Hospital, Antwerp, Belgium., Genovese G; Broad Institute of MIT and Harvard, Cambridge, MA, USA., McCarroll S; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Del-Favero J; VIB Center for Molecular Neurology, Universiteitsplein 1, Antwerp, Belgium and Multiplicom N.V., Galileilaan 18, Niel, Belgium., Adolfsson R; Department of Clinical Sciences and Psychiatry, University of Umeå, Umeå, Sweden. rolf.adolfsson@umu.se., Sullivan PF; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. pfsulliv@med.unc.edu.; Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. pfsulliv@med.unc.edu.; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. pfsulliv@med.unc.edu. |
| Abstrakt: |
We searched for genetic causes of major psychiatric disorders (bipolar disorder, schizoaffective disorder, and schizophrenia) in a large, densely affected pedigree from Northern Sweden that originated with three pairs of founders born around 1650. We applied a systematic genomic approach to the pedigree via karyotyping (N = 9), genome-wide SNP arrays (N = 418), whole-exome sequencing (N = 26), and whole-genome sequencing (N = 10). Comprehensive analysis did not identify plausible variants of strong effect. Rather, pedigree cases had significantly higher genetic risk scores compared to pedigree and community controls. |
