| pubmed-article:18056542 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C0041427 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C2347026 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C0370003 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C0036341 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C0870071 | lld:lifeskim |
| pubmed-article:18056542 | lifeskim:mentions | umls-concept:C1948020 | lld:lifeskim |
| pubmed-article:18056542 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:18056542 | pubmed:dateCreated | 2007-12-6 | lld:pubmed |
| pubmed-article:18056542 | pubmed:abstractText | The use of endophenotypes, biological traits that increase the liability to a disorder, represents one strategy to facilitate the detection of susceptibility genes for complex behavioral disorders such as schizophrenia. Establishing that a candidate trait is both heritable and linked genetically to schizophrenia is integral to its validity as an endophenotypic marker. Neurocognitive deficits are among the most promising indicators of increased risk for schizophrenia; however, it is not clear to what extent these deficits are genetically linked to the disorder. | lld:pubmed |
| pubmed-article:18056542 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18056542 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18056542 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18056542 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:18056542 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18056542 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:18056542 | pubmed:issn | 1538-3636 | lld:pubmed |
| pubmed-article:18056542 | pubmed:author | pubmed-author:ShamPakP | lld:pubmed |
| pubmed-article:18056542 | pubmed:author | pubmed-author:MurrayRobinR | lld:pubmed |
| pubmed-article:18056542 | pubmed:author | pubmed-author:EttingerUlric... | lld:pubmed |
| pubmed-article:18056542 | pubmed:author | pubmed-author:ToulopoulouTi... | lld:pubmed |
| pubmed-article:18056542 | pubmed:author | pubmed-author:RijsdijkFruhl... | lld:pubmed |
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| pubmed-article:18056542 | pubmed:author | pubmed-author:Hua-HallMeiM | lld:pubmed |
| pubmed-article:18056542 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18056542 | pubmed:volume | 64 | lld:pubmed |
| pubmed-article:18056542 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18056542 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18056542 | pubmed:pagination | 1348-55 | lld:pubmed |
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| pubmed-article:18056542 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:18056542 | pubmed:articleTitle | Substantial genetic overlap between neurocognition and schizophrenia: genetic modeling in twin samples. | lld:pubmed |
| pubmed-article:18056542 | pubmed:affiliation | Department of Psychiatry, Harvard Medical School, Boston, Massachusetts, USA. t.toulopoulou@iop.kcl.ac.uk | lld:pubmed |
| pubmed-article:18056542 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18056542 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18056542 | pubmed:publicationType | Twin Study | lld:pubmed |
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