Identification of FOXP2 truncation as a novel cause of developmental speech and language deficits.

ABSTRACT: FOXP2, the first gene to have been implicated in a developmental communication disorder, offers a unique entry point into neuromolecular mechanisms influencing human speech and language acquisition. In multiple members of the well-studied KE family, a heterozygous missense mutation in FOXP2 causes problems in sequencing muscle movements required for articulating speech (developmental verbal dyspraxia), accompanied by wider deficits in linguistic and grammatical processing. Chromosomal rearrangements involving this locus have also been identified. Analyses of FOXP2 coding sequence in typical forms of specific language impairment (SLI), autism, and dyslexia have not uncovered any etiological variants. However, no previous study has performed mutation screening of children with a primary diag

SUBMITTER: MacDermot KD 

PROVIDER: S-EPMC1196445 | biostudies-literature | 2005 Jun

REPOSITORIES: biostudies-literature