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dc.contributor.authorPettigrew, Kerry A
dc.contributor.authorFajutrao Valles, Samuelle F
dc.contributor.authorMoll, Kristina
dc.contributor.authorNorthstone, Kate
dc.contributor.authorRing, Susan
dc.contributor.authorPennell, Craig
dc.contributor.authorWang, Carol
dc.contributor.authorLeavett, Ruth
dc.contributor.authorHayiou-Thomas, Marianna E
dc.contributor.authorThompson, Paul
dc.contributor.authorSimpson, Nuala H
dc.contributor.authorFisher, Simon E
dc.contributor.authorWhitehouse, Andrew J O
dc.contributor.authorSnowling, Margaret J
dc.contributor.authorNewbury, Dianne F
dc.contributor.authorParacchini, Silvia
dc.contributor.authorSLI Consortium
dc.date.accessioned2015-04-08T10:31:02Z
dc.date.available2015-04-08T10:31:02Z
dc.date.issued2015-04-23
dc.identifier.citationPettigrew , K A , Fajutrao Valles , S F , Moll , K , Northstone , K , Ring , S , Pennell , C , Wang , C , Leavett , R , Hayiou-Thomas , M E , Thompson , P , Simpson , N H , Fisher , S E , Whitehouse , A J O , Snowling , M J , Newbury , D F , Paracchini , S & SLI Consortium 2015 , ' Lack of replication for the myosin-18B association with mathematical ability in independent cohorts ' , Genes, Brain and Behavior , vol. 14 , no. 4 , pp. 369-376 . https://doi.org/10.1111/gbb.12213en
dc.identifier.issn1601-1848
dc.identifier.otherPURE: 176256663
dc.identifier.otherPURE UUID: 3ec17f49-00bb-484d-b70c-6b36663e39e2
dc.identifier.otherPubMed: 25778778
dc.identifier.otherScopus: 84928304900
dc.identifier.otherORCID: /0000-0001-9934-8602/work/60428074
dc.identifier.otherWOS: 000353405000006
dc.identifier.urihttps://hdl.handle.net/10023/6445
dc.descriptionSP is a Royal Society University Research Fellow. This specific study in the ALSPAC cohort was supported by a MRC grant to SP [grant number G0800523/8647]. Support to the analysis was provided by the St Andrews Bioinformatics Unit funded by the Wellcome Trust [grant 097831/Z/11/Z].en
dc.description.abstractTwin studies indicate that dyscalculia (or mathematical disability) is caused partly by a genetic component, which is yet to be understood at the molecular level. Recently, a coding variant (rs133885) in the myosin-18B gene was shown to be associated with mathematical abilities with a specific effect among children with dyslexia. This association represents one of the most significant genetic associations reported to date for mathematical abilities and the only one reaching genome-wide statistical significance. We conducted a replication study in different cohorts to assess the effect of rs133885 maths-related measures. The study was conducted primarily using the Avon Longitudinal Study of Parents and Children (ALSPAC), (N = 3819). We tested additional cohorts including the York Cohort, the Specific Language Impairment Consortium (SLIC) cohort and the Raine Cohort, and stratified them for a definition of dyslexia whenever possible. We did not observe any associations between rs133885 in myosin-18B and mathematical abilities among individuals with dyslexia or in the general population. Our results suggest that the myosin-18B variant is unlikely to be a main factor contributing to mathematical abilities.
dc.language.isoeng
dc.relation.ispartofGenes, Brain and Behavioren
dc.rights© 2015 The Authors. Genes, Brain and Behavior published by International Behavioural and Neural Genetics Society and John Wiley & Sons Ltd. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en
dc.subjectDyscalculiaen
dc.subjectDyslexiaen
dc.subjectGenetic associationen
dc.subjectCognitive abilitiesen
dc.subjectNeurodevelopmental disordersen
dc.subjectALSPACen
dc.subjectR Medicineen
dc.subjectRC0321 Neuroscience. Biological psychiatry. Neuropsychiatryen
dc.subject3rd-DASen
dc.subject.lccRen
dc.subject.lccRC0321en
dc.titleLack of replication for the myosin-18B association with mathematical ability in independent cohortsen
dc.typeJournal articleen
dc.contributor.sponsorThe Wellcome Trusten
dc.description.versionPublisher PDFen
dc.contributor.institutionUniversity of St Andrews. School of Medicineen
dc.contributor.institutionUniversity of St Andrews. Biomedical Sciences Research Complexen
dc.identifier.doihttps://doi.org/10.1111/gbb.12213
dc.description.statusPeer revieweden
dc.identifier.grantnumber097831/z/11/zen


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