{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T00:11:39Z","timestamp":1790381499624,"version":"4.1.0"},"reference-count":82,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,12,7]],"date-time":"2012-12-07T00:00:00Z","timestamp":1354838400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Genes Brain and Behavior"],"published-print":{"date-parts":[[2013,2]]},"abstract":"<jats:p><jats:bold>Analysis of genetic linkage to dyslexia was performed using 133,165 array\u2010based <jats:styled-content style=\"fixed-case\">SNPs<\/jats:styled-content> genotyped in 718 persons from 101 dyslexia\u2010affected families. Results showed five linkage peaks with lod scores &gt;2.3 (4q13.1, 7q36.1\u2010q36.2, 7q36.3, 16p12.1, and 17q22). Of these five regions, three have been previously implicated in dyslexia (4q13.1, 16p12.1, and 17q22), three have been implicated in attention\u2010deficit hyperactivity disorder (<jats:styled-content style=\"fixed-case\">ADHD<\/jats:styled-content>, which highly co\u2010occurs with dyslexia; 4q13.1, 7q36.3, 16p12.1) and four have been implicated in autism (a condition characterized by language deficits; 7q36.1\u2010q36.2, 7q36.3, 16p12.1, and 17q22). These results highlight the reproducibility of dyslexia linkage signals, even without formally significant lod scores, and suggest dyslexia predisposing genes with relatively major effects and locus heterogeneity. The largest lod score (2.80) occurred at 17q22 within the <jats:italic><jats:styled-content style=\"fixed-case\">MSI2<\/jats:styled-content><\/jats:italic> gene, involved in neuronal stem cell lineage proliferation. Interestingly, the 4q13.1 linkage peak (lod 2.34) occurred immediately upstream of the <jats:italic><jats:styled-content style=\"fixed-case\">LPHN3<\/jats:styled-content><\/jats:italic> gene, recently reported both linked and associated with <jats:styled-content style=\"fixed-case\">ADHD<\/jats:styled-content>. Separate analyses of larger pedigrees revealed lods &gt;2.3 at 1\u20133 regions per family; one family showed strong linkage (lod 2.9) to a known dyslexia locus (18p11) not detected in our overall data, demonstrating the value of analyzing single large pedigrees. Association analysis identified no <jats:styled-content style=\"fixed-case\">SNPs<\/jats:styled-content> with genome\u2010wide significance, although a borderline significant <jats:styled-content style=\"fixed-case\">SNP<\/jats:styled-content> (<jats:italic>P<\/jats:italic>\u2009=\u20096\u2009\u00d7\u200910<jats:sup>\u20137<\/jats:sup>) occurred at 5q35.1 near <jats:italic><jats:styled-content style=\"fixed-case\">FGF18<\/jats:styled-content><\/jats:italic>, involved in laminar positioning of cortical neurons during development. We conclude that dyslexia genes with relatively major effects exist, are detectable by linkage analysis despite genetic heterogeneity, and show substantial overlapping predisposition with <jats:styled-content style=\"fixed-case\">ADHD<\/jats:styled-content> and autism.<\/jats:bold><\/jats:p>","DOI":"10.1111\/gbb.12003","type":"journal-article","created":{"date-parts":[[2012,11,29]],"date-time":"2012-11-29T01:07:31Z","timestamp":1354151251000},"page":"56-69","source":"Crossref","is-referenced-by-count":44,"title":["Dense\u2010map genome scan for dyslexia supports loci at 4q13, 16p12, 17q22; suggests novel locus at 7q36"],"prefix":"10.1111","volume":"12","author":[{"given":"L. 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