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CARNEY CENTRE NEWS

Last year's conference was a great success. Planning for this year's meeting is underway. Please diary the above date, and let us know if you would like to present at our one-day symposium, or be added to the mailing list. More details available here, and although there is no cost we ask you to register for the meeting.

NEW RESEARCH FROM THE CENTRE

McHugh, P.M., Deng, X., Joyce, P.R., Kennedy, M.A. (2010) A polymorphism of the GTP cyclohydrolase I feedback regulator gene alters transcriptional activity and may affect response to selective serotonin reuptake inhibitor antidepressants. The Pharmacogenomics Journal (In press).

Stamp, L.K., Chapman, P.T., O’Donnell, J.L., Zhang, M., James, J., Frampton, C., Barclay, M.L., Kennedy, M.A., Roberts, R.L. (2010) Polymorphisms within the folate pathway predict folate concentrations but are not associated with disease activity in rheumatoid arthritis patients on methotrexate. Pharmacogenetics and Genomics (In press).

Glubb, D.M., McHugh, P.C., Deng, S., Joyce,P.R., Kennedy, M.A. (2009) Association of a functional polymorphism in the adrenomedullin gene (ADM) with response to paroxetine. Pharmacogenomics Journal. 10, 126-133. In this work we describe gene expression changes induced by an antidepressant in a cultured neural cells. One of the most interesting expression changes observed was for a small protein hormone called adrenomedullin. Further investigation showed the gene for this protein may have a modest effect on patient responses to this antidepressant.

McHugh, P.M., Rogers, G.R., Glubb, D.M., Allington, M., Joyce, P.R., Kennedy, M.A. (2009) Proteomic analysis of rat hippocampus exposed to the antidepressant paroxetine. J Psychopharmacol. Apr 3. [Epub ahead of print]. This work is a preliminary exploration of the effect on protein patterns in the hippocampus after exposure to the antidepressant paroxetine. We identified a range of proteins that showed upregulation or downregulation of several proteins. The functions of these proteins may inform about aspects of antdidepressant action in the brain.

Glubb, D.M., Joyce, P.R., Kennedy, M.A. (2009) Expression and association analyses of promoter variants of the neurogenic gene HES6, a candidate gene for mood disorder susceptibility and antidepressant response. Neurosci. Let. 460, 1985-190. This study further explored a gene that showed expression changes in cultured brain cells exposed to the antidepressant paroxetine. We found that genetic variability in the control regions of the gene affected expression, but that these variants were not associated with risk of mood disorders or response to antidepressant drugs.

McHugh, P.M., Rogers,G.M., Glubb, D.M., Allington, M.D., Hughes, M., Joyce, P.R., and Kennedy, M.A. (2008) Downregulation of Cyclin D1 (Ccnd1) and Hairy Enhancer of Split 6 (Hes6) in rat hippocampus after chronic exposure to the antidepressant paroxetine. Acta Neuropsychiatrica 20, 307-313. This study explored gene expression changes in the brain induced by an antidepressant drugs, and identified two genes of possible importance to the action of these drugs.

Clark, DWJ, Ashton, JA, Wallace, AK, Zhou, L, Kennedy, MA. (2008) Pharmacogenetic investigation using a pharmacovigilance database. PharmacoVigilance Review 2, 9-13. David Clark and colleagues describe a pilot pharmacogenetic study in the pharmacovigilance database of the New Zealand Intensive Medicines Monitoring Programme.

Roberts,R.L, Gearry,R., Sies,C., George,P., Burt,M., Marinaki,A., Barclay,M., Kennedy, M.A. (2008). Trinucleotide repeat variants in the promoter of the thiopurine S-methyltransferase gene of patients exhibiting ultra-high enzyme activity. Pharmacogenetics and Genomics 18, 434-438. Genetic analysis of rare patients showing very high activity of an enzyme called TPMT, important in breaking down drugs used in treatment of inflammatory bowel disease and leukaemia, uncovered a subtle difference in the gene sequence which appears to result in high activity.

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