DYX4, INCLUDED
READING DISABILITY, SPECIFIC, 1 DYSLEXIA, SUSCEPTIBILITY TO, 4, INCLUDED
DYSLEXIA, SUSCEPTIBILITY TO, 7, INCLUDED
WORD-BLINDNESS, CONGENITAL
DYX7, INCLUDED
DYX1
Dyslexia is a disorder manifested by difficulty learning to read despite conventional instruction, adequate intelligence, and sociocultural opportunity. It is among the most common neurodevelopmental disorders, with a prevalence of 5 to 12%. Although there is evidence for ... Dyslexia is a disorder manifested by difficulty learning to read despite conventional instruction, adequate intelligence, and sociocultural opportunity. It is among the most common neurodevelopmental disorders, with a prevalence of 5 to 12%. Although there is evidence for familial clustering and heritability, the disorder is considered a complex multifactorial trait (Schumacher et al., 2007). - Genetic Heterogeneity of Susceptibility to Dyslexia Additional dyslexia susceptibility loci include DYX2 (600202) on chromosome 6p21.1, DYX3 (604254) on chromosome 2p16-p15, DYX5 (606896) on chromosome 3p12-q13, DYX6 (606616) on chromosome 18p11.2, DYX8 (608995) on chromosome 1p36-p34, and DYX9 (300509) on chromosome Xq27.3. See MAPPING for other possible dyslexia susceptibility loci.
Shaywitz et al. (1992) challenged the view of dyslexia as a biologically based disorder distinct from other less specific reading problems. According to this view, reading ability was considered to follow a bimodal distribution, with dyslexia as the ... Shaywitz et al. (1992) challenged the view of dyslexia as a biologically based disorder distinct from other less specific reading problems. According to this view, reading ability was considered to follow a bimodal distribution, with dyslexia as the lower mode. Shaywitz et al. (1992) contended that reading ability follows a normal distribution, with dyslexia at the lower end of the continuum. They presented data they interpreted as supporting their hypothesis. The argument was reminiscent of that which surrounded the genetics of essential hypertension (145500) 30 years earlier. Merzenich et al. (1996) and Tallal et al. (1996) described adaptive training exercises mounted as computer 'games' which demonstrated fundamental aspects of language-based learning impairment and suggested an approach to therapy. The work was based on evidence that language-based learning impairment (LLI) results from a basic deficit in processing rapidly changing sensory inputs. Specifically, LLI children commonly cannot identify fast elements embedded in ongoing speech that have durations in the range of a few tens of milliseconds, a critical time frame over which many phonetic contrasts are signaled. Normally, exposure to a specific language alters an infant's phonetic perceptions within the first months of life, leading to the setting of prototypic phonetic representations, the building blocks on which a child's native language develops. LLI is thought to represent a phonologic processing deficit. Merzenich et al. (1996) and Tallal et al. (1996) found that LLI children receiving extensive daily training over a period of weeks with listening exercises in which all speech was translated into a synthetic form showed improvement in their 'temporal processing' skills. From these studies, the authors concluded that there may be no fundamental defect in the learning machinery in most dyslexic children. Their conclusion suggests in turn that the physical differences and distributed functional response differences revealed in evoked potential and imaging studies of the brain of LLI individuals may be effects of the learning histories of these children. Furthermore, it may imply that inherited factors contributing to the origin of LLI may relate to the initiation of a scenario that embeds, through learning, a defective representation of speech phonetics, and does not necessarily mean that these children have irreversible defects in the molecular and cellular elements of the learning machinery of their brains. Svensson et al. (2011) reported a large 6-generation Swedish family in which 16 adults and 6 children (35% of total family members) had dyslexia. Ten family members had an uncertain diagnosis, and thirty family members had normal reading skills. All family members showed normal educational achievement. Males were more often affected than females. Genomewide linkage analysis did not identify a candidate region, and previous linkage studies to various candidate loci were not replicated. The studies suggested that the transmission of dyslexia in this family was not due to a highly penetrant major gene, but Svensson et al. (2011) noted that the power may have been too small to confirm linkage to genes with small or moderate effects.