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This study focuses on the stability of dyslexia status from Grade 2 to Grade 8 in four groups: (a) no dyslexia in either grade (no-dyslexia, n = 127); (b) no dyslexia in Grade 2 but dyslexia in Grade 8 (late-emerging, n = 18); (c) dyslexia in Grade 2 but not in Grade 8 (resolving, n = 15); and (d) dyslexia in both grades (persistent-dyslexia, n = 22). We examined group differences from age 3.5 to age 14 in (a) reading, vocabulary, phonology, letter knowledge, rapid naming, IQ, verbal memory; (b) familial and environmental risk and supportive factors; and (c) parental skills in reading, phonology, rapid naming, verbal memory, and vocabulary. Our findings showed group differences both in reading and cognitive skills of children as well as their parents. Parental education, book-reading frequency, and children's IQ, however, did not differentiate the groups. The children in the persistent-dyslexia group exhibited widespread language and cognitive deficits across development. Those in the resolving group had problems in language and cognitive skills only prior to school entry. In the late-emerging group, children showed clearly compromised rapid naming. Additionally, their parents had the most severe difficulties in rapid naming, a finding that suggests strong genetic liability. The findings show instability in the diagnosis of dyslexia. The members of the late-emerging group did not have a distinct early cognitive profile, so late-emerging dyslexia appears difficult to predict. Indeed, these children are at risk of not being identified and not receiving required support. This study suggests the need for continued monitoring of children's progress in literacy after the early school years. [ABSTRACT FROM AUTHOR]

Children at risk for familial dyslexia (n = 107) and their controls (n = 93) have been followed from birth to school entry in the Jyvaskyla Longitudinal study of Dyslexia (JLD) on developmental factors linked to reading and dyslexia. At the point of school entry, the majority of the at-risk children displayed decoding ability that fell at least 1 SD below the mean of the control group. Measures of speech processing were the earliest indices to show both group differences in infancy and also significant predictive associations with reading acquisition. A number of measures of language, including phonological and morphological skill collected repeatedly from age three, revealed group differences and predictive correlations. Both the group differences and the predictive associations to later language and reading ability strengthened as a function of increasing age. The predictions, however, tend to be stronger and the spectrum of significant correlations wider in the at-risk group. These results are crucial to early identification and intervention of dyslexia in at-risk children. [ABSTRACT FROM AUTHOR]

Emerging phonological awareness was compared in two groups of 3.5-year-old children belonging to the Jyväskylä Longitudinal Study of Dyslexia (JLD): children with familial risk of dyslexia (at-risk group n = 98) and children without such risk (control group n = 91). Four computer animated tasks were used: Word-level and Syllable-level Segment Identification, Synthesis, and Continuation of Phonological Units. The control group children manifested higher mastery than children in the at-risk group in phonological awareness, and the proportion of children with a low phonological awareness mean score was 2.5 times higher in the at-risk group than in the control group. In both groups, phonological awareness at 3.5 years was predicted by early language skills assessed between 14 and 26 months of age, and it was also associated with concurrent language. The difference between the at-risk and control group at 3.5-year in phonological awareness remained significant, even when the effect of other language skills such as productive and receptive vocabulary, and mastery of inflections, measured both at earlier ages and concurrently were controlled for. Our findings indicate that familial risk for dyslexia is reliably reflected in emerging phonological awareness already at this early age and it can be assessed independently of other language skills. [ABSTRACT FROM AUTHOR]

Developmental dyslexia, or reading disability, is a multigenic complex disease for which at least five loci, i.e. DYX1–3 and DYX5–6, have been clearly identified from the human genome. To date, DYX1C1 is the only dyslexia candidate gene cloned. We have previously reported linkage to 2p11 and 7q32 in 11 Finnish pedigrees. Here, we report the fine mapping of the approximately 40-cM linked region from chromosome 2 as we increased marker density to one per 1.8 cM. Linkage was supported with the highest NPL score of 3.0 (P=0.001) for marker D2S2216. Association analysis using the six pedigrees showing linkage pointed to marker D2S286/rs3220265 (P value <0.001) in the near vicinity of D2S2216. We went on to further characterise this ~15-cM candidate region (D2S2110-D2S2181) by adding six SNPs covering ~670 kb centred at D2S286/rs3220265. A haplotype pattern could no longer be observed in this region, which was therefore excluded from the candidate area. This also excluded the TACR1 (tachykinin receptor 1) gene, located at marker D2S286. The dyslexia candidate region on 2p11 is, therefore, now limited to the chromosomal area D2S2116-D2S2181, which is ~12 Mbp of human sequence and is at a distinct location from the previously reported DYX3 locus, raising the possibility of two distinct loci on chromosome 2p. [ABSTRACT FROM AUTHOR]