Abstract
Background: There is sufficient evidence that interference of dopaminergic neurotransmission contributes to the therapeutic effects of antidepressants in unipolar and bipolar depression. Methods: Hamilton depression rating scale (HAMD 17) scores of 163 at least moderately ill patients with major depressive disorders were used to establish treatment response. HAMD 17 score status was measured before initiation, after two weeks, and after four weeks of treatment with various antidepressants. The possible association between response and genotype in a total of 14 variants of dopamine neurotransmission-related proteins was investigated. Results: DRD4 rs11246226 CA heterozygous patients were found with a greater improvement of HAMD 17 score when compared to homozygous C patients during 0–2 weeks and 0–4 weeks. Patients with MAOB rs1799836 heterozygous GA and homozygous A also demonstrated improved scores during 2–4 weeks and 0–4 weeks. Conclusions: The results are preliminary due to the limited population size and the small number of variants. Further research into the involvement of habenular dopamine D4 receptors in the antidepressant response is desirable.
Highlights
IntroductionAntidepressants increase the extracellular concentration of monoamines within the brain by inhibiting their reuptake transporters (e.g., tricyclic antidepressants) or by catabolizing enzyme monoamine oxidase (e.g., MAO inhibitors)
Targeting this etiological pathway derives from the monoamine hypothesis of depression, where depression stems from the deficiency in transmissions in monoamine systems [2]
We investigated the possible existence of associations between genotypes of variants of genes encoding dopaminergic neurotransmission proteins and the response to antidepressant treatment of patients with major depressive disorder who had for at least 6 months been off treatment
Summary
Antidepressants increase the extracellular concentration of monoamines within the brain by inhibiting their reuptake transporters (e.g., tricyclic antidepressants) or by catabolizing enzyme monoamine oxidase (e.g., MAO inhibitors). Targeting this etiological pathway derives from the monoamine hypothesis of depression, where depression stems from the deficiency in transmissions in monoamine systems [2]. By focusing on dopaminergic neurotransmission, it may provide further insight into the personalised management of antidepressant medication [4,5]. There is sufficient evidence that interference of dopaminergic neurotransmission contributes to the therapeutic effects of antidepressants in unipolar and bipolar depression
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