| pubmed-article:16984965 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C0035648 | lld:lifeskim |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C0036341 | lld:lifeskim |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C0005586 | lld:lifeskim |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C2266276 | lld:lifeskim |
| pubmed-article:16984965 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:16984965 | pubmed:issue | 21 | lld:pubmed |
| pubmed-article:16984965 | pubmed:dateCreated | 2006-10-17 | lld:pubmed |
| pubmed-article:16984965 | pubmed:abstractText | The variability in phenotypic presentations and the lack of consistency of genetic associations in mental illnesses remain a major challenge in molecular psychiatry. Recently, it has become increasingly clear that altered promoter DNA methylation could play a critical role in mediating differential regulation of genes and in facilitating short-term adaptation in response to the environment. Here, we report the investigation of the differential activity of membrane-bound catechol-O-methyltransferase (MB-COMT) due to altered promoter methylation and the nature of the contribution of COMT Val158Met polymorphism as risk factors for schizophrenia and bipolar disorder by analyzing 115 post-mortem brain samples from the frontal lobe. These studies are the first to reveal that the MB-COMT promoter DNA is frequently hypomethylated in schizophrenia and bipolar disorder patients, compared with the controls (methylation rate: 26 and 29 versus 60%; P=0.004 and 0.008, respectively), particularly in the left frontal lobes (methylation rate: 29 and 30 versus 81%; P=0.003 and 0.002, respectively). Quantitative gene-expression analyses showed a corresponding increase in transcript levels of MB-COMT in schizophrenia and bipolar disorder patients compared with the controls (P=0.02) with an accompanying inverse correlation between MB-COMT and DRD1 expression. Furthermore, there was a tendency for the enrichment of the Val allele of the COMT Val158Met polymorphism with MB-COMT hypomethylation in the patients. These findings suggest that MB-COMT over-expression due to promoter hypomethylation and/or hyperactive allele of COMT may increase dopamine degradation in the frontal lobe providing a molecular basis for the shared symptoms of schizophrenia and bipolar disorder. | lld:pubmed |
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| pubmed-article:16984965 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16984965 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16984965 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16984965 | pubmed:status | MEDLINE | lld:pubmed |
