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  Developmental changes within the genetic architecture of social communication behaviour: A multivariate study of genetic variance in unrelated individuals

St Pourcain, B., Eaves, L. J., Ring, S. M., Fisher, S. E., Medland, S., Evans, D. M., et al. (2018). Developmental changes within the genetic architecture of social communication behaviour: A multivariate study of genetic variance in unrelated individuals. Biological Psychiatry, 83(7), 598-606. doi:10.1016/j.biopsych.2017.09.020.

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StPourcain_etal_2018.pdf (Verlagsversion), 299KB
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his is an open access article under the CC BY license ( http://creativecommons.org/licenses/by/4.0/

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St Pourcain, Beate1, 2, 3, 4, Autor           
Eaves, Lindon J.5, Autor
Ring, Susan M.2, 6, Autor
Fisher, Simon E.1, 3, Autor           
Medland, Sarah7, Autor
Evans, David M.2, 8, Autor
Smith, George Davey2, 6, Autor
Affiliations:
1Language and Genetics Department, MPI for Psycholinguistics, Max Planck Society, ou_792549              
2MRC Integrative Epidemiology Unit (MRC IEU), University of Bristol, Bristol, UK, ou_persistent22              
3Donders Institute for Brain, Cognition and Behaviour, External Organizations, ou_55236              
4Population genetics of human communication, MPI for Psycholinguistics, Max Planck Society, Wundtlaan 1, 6525 XD Nijmegen, NL, ou_2579694              
5 Department of Human and Molecular Genetics, Institute for Psychiatric and Behavioral Genetics, Commonwealth University School of Medicine, Richmond, Virginia, USA, ou_persistent22              
6School of Social and Community Medicine, University of Bristol, Bristol, UK, ou_persistent22              
7Psychiatric Genetics, QIMR Berghofer Medical Research Institute, Queensland, Australia, ou_persistent22              
8University of Queensland Diamantina Institute, Translational Research Institute, University of Queensland, Queensland, Australia, ou_persistent22              

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 Zusammenfassung: Background: Recent analyses of trait-disorder overlap suggest that psychiatric dimensions may relate to distinct sets of genes that exert their maximum influence during different periods of development. This includes analyses of social-communciation difficulties that share, depending on their developmental stage, stronger genetic links with either Autism Spectrum Disorder or schizophrenia. Here we developed a multivariate analysis framework in unrelated individuals to model directly the developmental profile of genetic influences contributing to complex traits, such as social-communication difficulties, during a ~10-year period spanning childhood and adolescence. Methods: Longitudinally assessed quantitative social-communication problems (N ≤ 5,551) were studied in participants from a UK birth cohort (ALSPAC, 8 to 17 years). Using standardised measures, genetic architectures were investigated with novel multivariate genetic-relationship-matrix structural equation models (GSEM) incorporating whole-genome genotyping information. Analogous to twin research, GSEM included Cholesky decomposition, common pathway and independent pathway models. Results: A 2-factor Cholesky decomposition model described the data best. One genetic factor was common to SCDC measures across development, the other accounted for independent variation at 11 years and later, consistent with distinct developmental profiles in trait-disorder overlap. Importantly, genetic factors operating at 8 years explained only ~50% of the genetic variation at 17 years. Conclusion: Using latent factor models, we identified developmental changes in the genetic architecture of social-communication difficulties that enhance the understanding of ASD and schizophrenia-related dimensions. More generally, GSEM present a framework for modelling shared genetic aetiologies between phenotypes and can provide prior information with respect to patterns and continuity of trait-disorder overlap

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Sprache(n): eng - English
 Datum: 2017-08-012016-09-172017-09-172017-09-282018
 Publikationsstatus: Erschienen
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 Ort, Verlag, Ausgabe: -
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 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: DOI: 10.1016/j.biopsych.2017.09.020
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Titel: Biological Psychiatry
  Andere : Biol. Psychiatry
Genre der Quelle: Zeitschrift
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Ort, Verlag, Ausgabe: New York : Elsevier
Seiten: - Band / Heft: 83 (7) Artikelnummer: - Start- / Endseite: 598 - 606 Identifikator: ISSN: 0006-3223
CoNE: https://pure.mpg.de/cone/journals/resource/954925384111