Dysbindin (DTNBP1)--a role in psychotic depression?

Previous studies yielded evidence for dysbindin (DTNBP1) to impact the pathogenesis of schizophrenia on the one hand and affective disorders such as bipolar or major depressive disorder (MDD) on the other. Thus, in the present study we investigated whether DTNBP1 variation was associated with psychotic depression as a severe clinical manifestation of MDD possibly constituting an overlapping phenotype between affective disorders and schizophrenia. A sample of 243 Caucasian inpatients with MDD (SCID-I) was genotyped for 12 SNPs spanning 92% of the DTNBP1 gene region.

Monoamine oxidase A variant influences antidepressant treatment response in female patients with Major Depression.

The monoamine oxidase A (MAO-A) has been suggested to be involved in the pathogenesis as well as the pharmacological treatment of Major Depression. In the present study, 340 patients with a Major Depressive Episode (f=194, m=146; DSM-IV) of Caucasian descent were genotyped for the functional MAO-A VNTR. The clinical response to antidepressive pharmacological treatment was assessed by weekly intra-individual changes of HAM-D-21 scores over six weeks.

Association of the COMT val158met variant with antidepressant treatment response in major depression.

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.