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Pharmacogenetics of Antidepressants: Is There a Magic Bullet for Treating Depression?

Min-Soo Lee

Depression is one of the most common mental disorders nowadays. Many
researchers in psychiatry have investigated the cause of depression. Unfortunately,
the problem of individual differences in response to antidepressant treatment still
lingers in the clinical field. For setting up the stage for the main topics in the later
part of this overview, I start introducing the topics of monoamine hypothesis, the
rôle of serotonin in causing clinical depression, as well as advents of antidepressants (briefly describing tricyclic antidepressants, the arrival of selective serotoninreuptake inhibitor, and novel antidepressants). Then, I introduce the concept of
pharmacogenetics, the candidate genes. Afterwards, I consider that genetic factors
are recognized to have an independent effect on drug responses. To demonstrate, I
highlight five gene studies ‒ serotonin transporter (5-HTT/SLC6A4), serotonin
receptor 2A (HTR2A), G-protein β3 subunit (GNB3), brain-derived neurotrophic
factor (BDNF), and tryptophan hydroxylase (TPH). But some of candidate gene
studies have been conducted, but results were not consistent. Since 2009, Genomewide Association Studies (GWAS) has provided further grounds for understanding
the pharmacogenetic mechanisms of antidepressants and depression treatment.
Further research and technological development are still needed.
Key Word antidepressants, monoamines, pharmacogenetics, Genome-wide Association Studies (GWAS)
Editorial Committe, Taiwanese Journal of Psychiatry
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