Editing Expressive language disorder (section)

===Developmental verbal dyspraxia===
In 1990, it was reported that the several generations of the [[KE family]] had [[developmental verbal dyspraxia]] and [[Apraxia#Types|orofacial praxis]] that were inherited in a typical [[autosomal dominant]] pattern.<ref name="Hurst 1990">{{cite journal | vauthors = Hurst JA, Baraitser M, Auger E, Graham F, Norell S | title = An extended family with a dominantly inherited speech disorder | journal = Developmental Medicine and Child Neurology | volume = 32 | issue = 4 | pages = 352–355 | date = April 1990 | pmid = 2332125 | doi = 10.1111/j.1469-8749.1990.tb16948.x | s2cid = 2654363 }}</ref> Further analysis traced this inheritance pattern back to mutations in the FOXP2 genes.<ref name="Vargha-Khadem 2005"/><ref name="Liégeois 2003">{{cite journal | vauthors = Liégeois F, Baldeweg T, Connelly A, Gadian DG, Mishkin M, Vargha-Khadem F | title = Language fMRI abnormalities associated with FOXP2 gene mutation | journal = Nature Neuroscience | volume = 6 | issue = 11 | pages = 1230–1237 | date = November 2003 | pmid = 14555953 | doi = 10.1038/nn1138 | s2cid = 31003547 }}</ref> These studies have allowed scientists to begin to investigate how changes to one gene can alter human communication.

FOXP2 is the first gene that has been identified that is specifically linked to speech and language production. Mutant alleles of the normal [[FOXP2]] gene have been found to be the cause of severe speech impairments.<ref name="Vargha-Khadem 2005">{{cite journal | vauthors = Vargha-Khadem F, Gadian DG, Copp A, Mishkin M | title = FOXP2 and the neuroanatomy of speech and language | journal = Nature Reviews. Neuroscience | volume = 6 | issue = 2 | pages = 131–138 | date = February 2005 | pmid = 15685218 | doi = 10.1038/nrn1605 | s2cid = 2504002 }}</ref>