Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Association of the COMT val158met Variant with Antidepressant Treatment Response in Major Depression|
|Citation:||Neuropsychopharmacology, 2008; 33(4):924-932|
|Publisher:||Elsevier Science Inc|
|Bernhard T Baune, Christa Hohoff, Klaus Berger, Anna Neumann, Sünke Mortensen, Tilmann Roehrs, Jürgen Deckert, Volker Arolt and Katharina Domschke|
|Abstract:||In several previous biochemical, pharmacological, and genetic studies, the catechol-O-methyltransferase (COMT) has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of affective disorders. In the present study, 256 patients with major depression (DSM-IV) of Caucasian descent were genotyped for the functional COMT val158met polymorphism and characterized for clinical response to antidepressive pharmacological treatment as measured by intra-individual changes of Hamilton Depression (HAM-D-21) scores over 6 weeks. The COMT 158val/val genotype conferred a significant risk of worse response after 4–6 weeks of antidepressant treatment in patients with major depression (week 4: p=0.003; week 5: p<0.0001; week 6: p<0.0001) after Bonferroni correction for multiple comparisons. The present results strongly point toward a negative influence of the higher activity COMT 158val/val genotype on antidepressant treatment response during the first 6 weeks of pharmacological treatment in major depression, possibly conferred by consecutively decreased dopamine availability. This finding suggests a potentially beneficial effect of an antidepressive add-on therapy with substances increasing dopamine availability individually tailored according to COMT val158met genotype.|
|Keywords:||major depression; catechol-O-methyltransferase; COMT val158met; polymorphism; antidepressants; treatment response|
|Rights:||© 2008 Nature Publishing Group. All rights reserved.|
|Appears in Collections:||Psychiatry publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.