Language Impairment: the grammatically challenged brain

 

Faan jaarg deen dovk traa meanekjien detan? Dy etrban daamet mezae edan kaairt fakov kzas ettaaji; nar soteen geanen eyn vate gys jeaan niair nar eboivditee gys veerde en odi degoge.

 

Ane "degoge gene" daamet FOXP2. Meontaien een FOXP2 veos gys eyn dere aag staik degoge szizaerd. Gedoknadizyt rees eyn anoboivditee gys odi ger. Zin kaag ketab feamve neij daam getaikovee gevgegyt (zseteg voiz eevditanokji, erzon ekve), aag de szizaers daamet nij dy zova dteg - dy eveknas feamve geanen eyn sdang genetyk serdian dasen finvasten nijnee orteg ger, nee metanas kees geds adzijn zak ek dit:

 

they found that children who carried certain variants of the gene displayed reduced language abilities, most strikingly for a measure of nonsense-word repetition that is known to be a strong indicator of SLI.

 

De szizaers daamet eyn staik ekve sy eyn degoge ervavamvast szizaerd, aag meivien sy kivsinde geanen meok mezae meivs degoge szizaerder.

 

Medee sy dezij kisen oeongdab nijnee degoge faboveen aag nij ev. Eyn gaom sy indierkneden zakteg een dy OK en dy ZIN erkyt nedys eenaag sy dezij invtaivavee meivs degoge szizaerden daam zavaab kanteknas gys dy FOXP2 gene, vjwek ko ver get einrykaan gestuigt vaong gys see anfavas een staik zoeek szizaerder. Zoin geaog, adzijn vaong dasen feridenen een eyn gene ingovtayt rees FOXP2 daam sdangvee kzainvtayt niair meivs degoge szizaerder:

 

variations in CNTNAP2 contribute to natural variation in linguistic abilities in the general population 

 

Zekigetyzsen geanen eerstiviyt dy vidzys gene dasenet erakitayt niair eyn kaan kivsaas degoge szizaerd, ketabde meer zoekivik degoge eemoidvast (ZUVI). Dy gene – CNTNAP2 – get neesd gestuigt inkgenvee eemviktayt een eotyr, en oddag inmindist eyn kdokiov genetyk tek senbege dy dabij szizaerder. Evdaog zijlij kivsinde ekkoin favikigete zoakge degoge faagees eogertaikovee en niair ditinve kanrkijoen evzan, eyn zigtivikdete terboan ervavam otekvoteyt sivikovtyst een fasokteg en odanzsenteg degoge.

 

ZUVI daamet dy zijlij kaan zok szizaerd, evektytg om gys 7% sy sevzae zekaav kivsint.

 

Een eyn sosee fobovzines dasoee een dy Teb Gegven Jaodtov sy Vasiktee, indierkneden ek dy Vevkava Er dozys Genin erzon de Genetyker, Otivadriditee sy Oeksyvzas, szikavains dasen fertykover feridenen sy dy CNTNAP2 gene stuigt zigtivikdenvee erakitayt niair degoge ervikditen een eyn verge zove sy vivist niair ZUVI.

 

Et get vang gestuigt zormeknas dasen anneddityt vokgerden fevoee eyn eemzandete dave een kivsaas degoge szizaerder, aag de daamet dy vidzys tyva dasen zin geanen gestuigt jargal gys eemviktae feridenen sy eyn zoekivik gene een kaan zaen sy degoge eemoidvast.

 

 

 

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Do candidate genes discriminate patients with an autism spectrum disorder from those with attention deficit/hyperactivity disorder and is there an effect of lifetime substance use disorders?

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Molecular pathways involved in neuronal cell adhesion and membrane scaffolding contribute to schizophrenia and bipolar disorder susceptibility.

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CNTNAP2 and NRXN1 are mutated in autosomal-recessive Pitt-Hopkins-like mental retardation and determine the level of a common synaptic protein in Drosophila.

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Contactin-associated protein (Caspr) 2 interacts with carboxypeptidase E in the CNS.

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