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

@article{Macdermot2005IdentificationOF,
  title={Identification of FOXP2 truncation as a novel cause of developmental speech and language deficits.},
  author={K Macdermot and Elena Bonora and Nuala Sykes and Anne-Marie Coupe and Cecilia S. L. Lai and Sonja C Vernes and Faraneh Vargha-Khadem and Fiona C. McKenzie and Robert L. Smith and Anthony P. Monaco and Simon E. Fisher},
  journal={American journal of human genetics},
  year={2005},
  volume={76 6},
  pages={1074-80}
}
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… CONTINUE READING
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