Interrelationship and familiality of dyslexia related quantitative measures.

Dyslexia is a complex gene-environment disorder with poorly understood etiology that affects about 5% of school-age children. Dyslexia occurs in all languages and is associated with a high level of social and psychological morbidity for the individual and their family; approximately 40-50% have persistent disability into adulthood. The core symptoms are word reading and spelling deficits, but several other cognitive components influence the core phenotype. A broad spectrum of dyslexia related phenotypes, including phonological decoding, phoneme awareness, orthographic processing, short-term memory, rapid naming and basic mathematical abilities, were investigated in large sample of 287 German dyslexia families. We explored the interrelationship between the component phenotypes using correlation and principal component analyses (PCA). In addition, we estimated familiality for phenotypes as well as for the factors suggested by PCA. The correlation between the component phenotypes varied between -0.1 and 0.7. The PCA resulted in three factors: a general dyslexia factor, a speed of processing factor and a mathematical abilities factor. The familiality estimates of single components and factors ranged between 0.25 and 0.63. Instead of analyzing single dyslexia-related components, multivariate analyses including factor analytic approaches may help in the identification of susceptibility genes.

Linkage analyses of chromosomal region 18p11-q12 in dyslexia.

Dyslexia is characterized as a significant impairment in reading and spelling ability that cannot be explained by low intelligence, low school attendance or deficits in sensory acuity. It is known to be a hereditary disorder that affects about 5% of school aged children, making it the most common of childhood learning disorders. Several susceptibility loci have been reported on chromosomes 1, 2, 3, 6, 15, and 18. The locus on chromosome 18 has been described as having the strongest influence on single word reading, phoneme awareness, and orthographic coding in the largest genome wide linkage study published to date (Fisher et al., 2002). Here we present data from 82 German families in order to investigate linkage of various dyslexia-related traits to the previously described region on chromosome 18p11-q12. Using two- and multipoint analyses, we did not find support for linkage of spelling, single word reading, phoneme awareness, orthographic coding and rapid naming to any of the 14 genotyped STR markers. Possible explanations for our non-replication include differences in study design, limited power of our study and overestimation of the effect of the chromosome 18 locus in the original study.

Visual information processing in dyslexic children.

OBJECTIVE: Several studies presented evidence for magnocellular deficits in dyslexics both in behavioural as well as in electrophysiological data of local electrode sites. We investigated two well-known paradigms (motion-onset and random-dot-kinematogram) with regard to global electrophysiological parameters. METHODS: Twenty-one-channel event-related potentials (ERPs) of 16 dyslectic and 15 control children were analyzed with reference-independent methods. For each paradigm quasi stable microstates were identified by means of a data-driven segmentation procedure and compared between both groups. RESULTS: Differences in global ERP responses between dyslexic and control children could be found for rapid moving gratings but not for the dot coherence. CONCLUSIONS: Dyslexic children seem to have some highly specific visual deficits in processing moving stimuli. These deficits can be related to the magnocellular system.