REVIEW

Genetics of dyslexia: the evolving landscape

Johannes Schumacher¹, Per Hoffmann², Christine Schmäl³, Gerd Schulte-Körne⁴, Markus M Nöthen²

¹ Institute of Human Genetics, University of Bonn, Bonn, Germany
² Department of Genomics, Life & Brain Centre, University of Bonn, Bonn, Germany
³ Division of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Mannheim, Germany
⁴ Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatic Medicine, University of Munich, Munich, Germany

Correspondence to:
Professor M M Nöthen
Department of Genomics, Life & Brain Centre, University of Bonn, Sigmund-Freud-Strasse 25, D-53105 Bonn, Germany; markus.noethen{at}uni-bonn.de

Dyslexia is among the most common neurodevelopmental disorders, with a prevalence of 5–12%. At the phenotypic level, various cognitive components that enable reading and spelling and that are disturbed in affected individuals can be distinguished. Depending on the phenotype dimension investigated, inherited factors are estimated to account for up to 80%. Linkage findings in dyslexia are relatively consistent across studies in comparison to findings for other neuropsychiatric disorders. This is particularly true for chromosome regions 1p34–p36, 6p21–p22, 15q21 and 18q11. Four candidate genes have recently been identified through systematic linkage disequilibrium studies in linkage region 6p21–p22, and through cloning approaches at chromosomal breakpoints. Results indicate that a disturbance in neuronal migration is a pathological correlate of dyslexia at the functional level. This review presents a summary of the latest insights into the genetics of dyslexia and an overview of anticipated future developments.

Abbreviations: ADHD, attention-deficit hyperactivity disorder; CNS, central nervous system; DCDC2, doublecortin domain containing protein 2; DYX1, dyslexia susceptibility 1; DYX9, dyslexia susceptibility 9; DYX1C1, dyslexia susceptibility 1 candidate 1; LD, linkage disequilibrium; QTL, quantitative trait loci; ROBO1, roundabout Drosophila homolog of 1; SSD, speech–sound disorder

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