| pubmed-article:18179893 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18179893 | lifeskim:mentions | umls-concept:C1422223 | lld:lifeskim |
| pubmed-article:18179893 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:18179893 | lifeskim:mentions | umls-concept:C0023745 | lld:lifeskim |
| pubmed-article:18179893 | lifeskim:mentions | umls-concept:C0004083 | lld:lifeskim |
| pubmed-article:18179893 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
| pubmed-article:18179893 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18179893 | pubmed:dateCreated | 2008-1-8 | lld:pubmed |
| pubmed-article:18179893 | pubmed:abstractText | Autism is a genetically complex neurodevelopmental syndrome in which language deficits are a core feature. We describe results from two complimentary approaches used to identify risk variants on chromosome 7 that likely contribute to the etiology of autism. A two-stage association study tested 2758 SNPs across a 10 Mb 7q35 language-related autism QTL in AGRE (Autism Genetic Resource Exchange) trios and found significant association with Contactin Associated Protein-Like 2 (CNTNAP2), a strong a priori candidate. Male-only containing families were identified as primarily responsible for this association signal, consistent with the strong male affection bias in ASD and other language-based disorders. Gene-expression analyses in developing human brain further identified CNTNAP2 as enriched in circuits important for language development. Together, these results provide convergent evidence for involvement of CNTNAP2, a Neurexin family member, in autism, and demonstrate a connection between genetic risk for autism and specific brain structures. | lld:pubmed |
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| pubmed-article:18179893 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18179893 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18179893 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18179893 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18179893 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:18179893 | pubmed:issn | 1537-6605 | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:AlarcónMarice... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:CantorRita... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:GeschwindDani... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:LedbetterDavi... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:NelsonStanley... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:WiglerMichael... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:AbrahamsBrett... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:StoneJennifer... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:MartinChrista... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:SebatJonathan... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:BomarJamee... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:DuvallJacquel... | lld:pubmed |
| pubmed-article:18179893 | pubmed:author | pubmed-author:PerederiyJuli... | lld:pubmed |
| pubmed-article:18179893 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18179893 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:18179893 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18179893 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18179893 | pubmed:pagination | 150-9 | lld:pubmed |
| pubmed-article:18179893 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:18179893 | pubmed:meshHeading | pubmed-meshheading:18179893... | lld:pubmed |
