% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Richards:151594,
      author       = {Richards, Alexander L and Pardiñas, Antonio F and
                      Frizzati, Aura and Tansey, Katherine E and Lynham, Amy J and
                      Holmans, Peter and Legge, Sophie E and Savage, Jeanne E and
                      Agartz, Ingrid and Andreassen, Ole A and Blokland, Gabriella
                      A M and Corvin, Aiden and Cosgrove, Donna and Degenhardt,
                      Franziska and Djurovic, Srdjan and Espeseth, Thomas and
                      Ferraro, Laura and Gayer-Anderson, Charlotte and Giegling,
                      Ina and van Haren, Neeltje E and Hartmann, Annette M and
                      Hubert, John J and Jönsson, Erik G and Konte, Bettina and
                      Lennertz, Leonhard and Olde Loohuis, Loes M and Melle,
                      Ingrid and Morgan, Craig and Morris, Derek W and Murray,
                      Robin M and Nyman, Håkan and Ophoff, Roel A and van Os, Jim
                      and Petryshen, Tracey L and Quattrone, Diego and Rietschel,
                      Marcella and Rujescu, Dan and Rutten, Bart P F and Streit,
                      Fabian and Strohmaier, Jana and Sullivan, Patrick F and
                      Sundet, Kjetil and Wagner, Michael and Escott-Price,
                      Valentina and Owen, Michael J and Donohoe, Gary and
                      O’Donovan, Michael C and Walters, James T R},
      title        = {{T}he {R}elationship {B}etween {P}olygenic {R}isk {S}cores
                      and {C}ognition in {S}chizophrenia},
      journal      = {Schizophrenia bulletin},
      volume       = {46},
      issn         = {0586-7614},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DZNE-2020-01178},
      pages        = {sbz061},
      year         = {2019},
      abstract     = {BackgroundCognitive impairment is a clinically important
                      feature of schizophrenia. Polygenic risk score (PRS) methods
                      have demonstrated genetic overlap between schizophrenia,
                      bipolar disorder (BD), major depressive disorder (MDD),
                      educational attainment (EA), and IQ, but very few studies
                      have examined associations between these PRS and cognitive
                      phenotypes within schizophrenia cases.MethodsWe combined
                      genetic and cognitive data in 3034 schizophrenia cases from
                      11 samples using the general intelligence factor g as the
                      primary measure of cognition. We used linear regression to
                      examine the association between cognition and PRS for EA,
                      IQ, schizophrenia, BD, and MDD. The results were then
                      meta-analyzed across all samples. A genome-wide association
                      studies (GWAS) of cognition was conducted in schizophrenia
                      cases.ResultsPRS for both population IQ (P = 4.39 ×
                      10–28) and EA (P = 1.27 × 10–26) were positively
                      correlated with cognition in those with schizophrenia. In
                      contrast, there was no association between cognition in
                      schizophrenia cases and PRS for schizophrenia (P = .39), BD
                      (P = .51), or MDD (P = .49). No individual variant
                      approached genome-wide significance in the
                      GWAS.ConclusionsCognition in schizophrenia cases is more
                      strongly associated with PRS that index cognitive traits in
                      the general population than PRS for neuropsychiatric
                      disorders. This suggests the mechanisms of cognitive
                      variation within schizophrenia are at least partly
                      independent from those that predispose to schizophrenia
                      diagnosis itself. Our findings indicate that this cognitive
                      variation arises at least in part due to genetic factors
                      shared with cognitive performance in populations and is not
                      solely due to illness or treatment-related factors, although
                      our findings are consistent with important contributions
                      from these factors.},
      keywords     = {Bipolar Disorder: genetics / Datasets as Topic / Depressive
                      Disorder, Major: genetics / Educational Status / Genome-Wide
                      Association Study / Humans / Intelligence: genetics /
                      Multifactorial Inheritance / Psychotic Disorders: genetics /
                      Schizophrenia: genetics},
      cin          = {AG Höglinger 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7442352},
      pubmed       = {pmid:31206164},
      doi          = {10.1093/schbul/sbz061},
      url          = {https://pub.dzne.de/record/151594},
}