Počet záznamů: 1  

Common Genetic Variation and Age of Onset of Anorexia Nervosa

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    0576271 - ÚOCHB 2024 RIV US eng J - Článek v odborném periodiku
    Watson, H. J. - Thornton, L. M. - Yilmaz, Z. - Baker, J. H. - Coleman, J. R. I. - Adan, R. A. H. - Alfredsson, L. - Andreassen, O. A. - Ask, H. - Berrettini, W. H. - Boehnke, M. - Boehm, I. - Boni, C. - Buehren, K. - Bulant, J. - Burghardt, R. - Chang, X. - Cichon, S. - Cone, R. D. - Courtet, P. - Crow, S. - Crowley, J. J. - Danner, U. N. - de Zwaan, M. - Dedoussis, G. - DeSocio, J. E. - Dick, D. M. - Dikeos, D. - Dina, C. - Šlachtová, Lenka - Bulik, C. M. … celkem 178 autorů
    Common Genetic Variation and Age of Onset of Anorexia Nervosa.
    Biological Psychiatry. Global Open Science. Roč. 2, č. 4 (2022), s. 368-378. ISSN 2667-1743
    Institucionální podpora: RVO:61388963
    Klíčová slova: genome-wide association * eating disorders * familial aggregation
    Obor OECD: Biochemistry and molecular biology
    Způsob publikování: Open access
    https://doi.org/10.1016/j.bpsgos.2021.09.001

    BACKGROUND: Genetics and biology may influence the age of onset of anorexia nervosa (AN). The aims of this study were to determine whether common genetic variation contributes to age of onset of AN and to investigate the genetic associations between age of onset of AN and age at menarche.METHODS: A secondary analysis of the Psychiatric Genomics Consortium genome-wide association study (GWAS) of AN was performed, which included 9335 cases and 31,981 screened controls, all from European ancestries. We conducted GWASs of age of onset, early-onset AN (,13 years), and typical-onset AN, and genetic correlation, genetic risk score, and Mendelian randomization analyses.RESULTS: Two loci were genome-wide significant in the typical-onset AN GWAS. Heritability estimates (single nucleotide polymorphism-h2) were 0.01-0.04 for age of onset, 0.16-0.25 for early-onset AN, and 0.17-0.25 for typical-onset AN. Early-and typical-onset AN showed distinct genetic correlation patterns with putative risk factors for AN. Specifically, early-onset AN was significantly genetically correlated with younger age at menarche, and typical-onset AN was significantly negatively genetically correlated with anthropometric traits. Genetic risk scores for age of onset and early-onset AN estimated from independent GWASs significantly predicted age of onset. Mendelian randomization analysis suggested a causal link between younger age at menarche and earlyonset AN.CONCLUSIONS: Our results provide evidence consistent with a common variant genetic basis for age of onset and implicate biological pathways regulating menarche and reproduction.
    Trvalý link: https://hdl.handle.net/11104/0345835

     
     
Počet záznamů: 1  

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