Absence of significant linkage between phonological coding dyslexia and chromosome 6p23-21.3, as determined by use of quantitative-trait methods: Confirmation of qualitative analyses

Citation
Tl. Petryshen et al., Absence of significant linkage between phonological coding dyslexia and chromosome 6p23-21.3, as determined by use of quantitative-trait methods: Confirmation of qualitative analyses, AM J HU GEN, 66(2), 2000, pp. 708-714
Citations number
20
Categorie Soggetti
Research/Laboratory Medicine & Medical Tecnology","Molecular Biology & Genetics
Journal title
AMERICAN JOURNAL OF HUMAN GENETICS
ISSN journal
00029297 → ACNP
Volume
66
Issue
2
Year of publication
2000
Pages
708 - 714
Database
ISI
SICI code
0002-9297(200002)66:2<708:AOSLBP>2.0.ZU;2-L
Abstract
We recently reported the absence of significant linkage of phonological cod ing dyslexia (PCD) to chromosome 6p23-p21.3 in 79 families with at least tw o affected siblings, even though linkage of dyslexia to this region has bee n found in four other independent studies. Whereas, in our previous analyse s, we used a qualitative (affected, unaffected, or uncertain) PCD phenotype , here we report a reanalysis of linkage to the chromosome 6p region, by us e of four quantitative measures of reading disability: phonological awarene ss, phonological coding, spelling, and rapid-automatized-naming (RAN) speed . The phonological-coding and spelling measures were highly correlated with each other and with the qualitative PCD phenotype, whereas the phonologica l-awareness and RAN-speed measures were only moderately correlated with the other measures. Using two-point and multipoint quantitative-trait sib-pair linkage analyses and variance-components analyses, we were unable to detec t significant evidence for a locus in the 6p23-p21.3 region influencing any of the quantitative reading measures, supporting our previous qualitative linkage results. The most likely explanation for our inability to detect li nkage between dyslexia and this region is that families with subtypes of dy slexia linked to this region are underrepresented in our sample, because of either chance or varying ascertainment criteria.