and autism have been described (e.g., Cox et al; 2003; Wassink et al., 2001; Winslow & Insel, 2002).
Localization and isolation of genes for language and learning disorders are difficult, but ongoing improvements in statistical analysis and molecular technology make it more likely that at least the more common and penetrant genes will be identified. Studies of dyslexia are particularly encouraging, with the replication of several localizations including 2p, 3c, 6p, 15q, and 18p (see Fisher & DeFries, 2002, for a recent review). A genome-wide scan of SLI produced possible linkages to 16q and 19q (SLIConsortium, 2002), but candidate gene studies of SPCH1 have been less clear. Suggestion of linkage to the region has been reported by O'Brien et al. (2003), but not in other studies, and direct analysis of the FOXP2 gene did not find mutations in any of the studies (e.g., Newbury et al., 2002). Analysis of surrounding markers by O'Brien et al. indicates that another gene or genes in the region around FOXP2 might be involved, however.
Some of the comorbidity between disorders may be explained by particular genes that may affect both phenotypes, such as a region of 13q affecting SLI and dyslexia (Bartlett et al., 2002) and a locus or loci in 6p affecting dyslexia and ADHD (Willcutt et al., 2002). Similarly, genome scans of ADHD have indicated possible linkages to 16p (Ogdie et al., 2003; Smalley et al., 2002) and 5p (Ogdie et al., 2003) in the same regions identified by autism studies (International Molecular Genetic Study of Autism Consortium, 2001; Liu et al., 2001; Philippe et al., 1999). Thus, finding the genes affecting any one of these disorders may not only reveal the pathogenesis of that condition, but could lead to the understanding of other language and learning disorders as well.
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