Evidence for a genetic aetiology in reading disability of twins

Abstract

Reading disability (dyslexia) is a major social, educational, and mental health problem. Although estimates of prevalence vary, up to 10-15% of school-age children have severe reading deficits in spite of average intelligence and adequate educational opportunity. That reading disability may have a constitutional basis has long been recognized, and results of twin and family studies suggest that one or more of its forms may be heritable; however, definitive evidence for a genetic aetiology has not been reported. Establishing a heritable basis for reading disability could suggest possible causes, give improved risk estimates, facilitate early diagnosis, and provide validity tests for ostensible subtypes. In this report, we apply a recently developed multiple regression analysis to data collected from a sample of 64 pairs of identical twins and 55 pairs of fraternal twins, in which at least one member of the pairs is reading disabled, and present evidence for a significant genetic aetiology.

DCDC2 is associated with reading disability and modulates neuronal development in the brain

“…Estimates of heritability range from 44% to 75% (5). The first RD susceptibility region, DYX1, was reported on chromosome 15 in 1983 (6).…”

Developmental dyslexia: an update

“…There is strong evidence (affected parent) for a genetic contribution to the disorder. According to twin studies, only certain reading related skills (phonological aspects of reading accuracy) are inherited and the heritability of the disorder is approximately 0.71 (Pennington et al 1991;Schulte-Korne 1996;DeFries et al 1987). When children of consanguineous marriages were examined for their reading disabilities, the rate of reading disabilities is higher in children of firstcousin parents than that of second-cousin or unrelated parents.…”

Further evidence that the KIAA0319 gene confers susceptibility to developmental dyslexia

“…Although the pathophysiology of DD is unknown, there is strong evidence that genes make a substantial contribution to individual variation in risk of DD, with twin studies reporting heritability estimates of up to 0.71. [1][2][3][4][5][6][7][8] Linkage studies have identified several genomic regions that may harbor susceptibility quantitative trait loci (QTL) for DD, and the most consistently replicated of these is DYX2, which lies on chromosome 6p22.2. 1,[9][10][11][12][13][14][15][16] A number of association studies have now been performed attempting to identify the DYX2 susceptibility locus.…”