| pubmed-article:20179754 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0025265 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0597198 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0681842 | lld:lifeskim |
| pubmed-article:20179754 | lifeskim:mentions | umls-concept:C0079809 | lld:lifeskim |
| pubmed-article:20179754 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:20179754 | pubmed:dateCreated | 2010-2-24 | lld:pubmed |
| pubmed-article:20179754 | pubmed:abstractText | Variation of the gene coding for D2 receptors (DRD2) has been associated with risk for schizophrenia and with working memory deficits. A functional intronic SNP (rs1076560) predicts relative expression of the two D2 receptors isoforms, D2S (mainly pre-synaptic) and D2L (mainly post-synaptic). However, the effect of functional genetic variation of DRD2 on striatal dopamine D2 signaling and on its correlation with prefrontal activity during working memory in humans is not known. | lld:pubmed |
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