The tolerability and response to antidepressants is affected by two fundamental processes, the metabolization of antidepressants and the interaction with other type of genes that are not metabolizing enzymes and that affect other mechanisms such as transport, etc. The genetic polymorphisms that affect genes for the metabolization of multiple antidepressants have already been described in the items of ""Metabolization of Antidepressants"".

In this technical report we study the genetic polymorphisms of several genes that interact with the antidepressants fluoxetine, citalopram and escitalopram and whose genotype is associated with a better or worse response to treatment. This technical report is associated with these three serotonin reuptake inhibitor antidepressants (SSRIs), however, it is extensible to many other antidepressants in this family. It is widely described that the genetic variability in the serotonergic system of the brain (that is, in the set of genes that affect the correct exposure and reaction of neurons to serotonin, a neurotransmitter that maintains mental equilibrium) has a very significant impact on the response to certain antidepressants. There are certain candidate genes in which this relevance has been studied for the pharmacogenetics of antidepressant medication, such as: 5-HT2A, 5-HT1A, 5-HTTLPR, MAOA, COMT, TPH2. In the genetic test of tellmeGen we study polymorphisms of genes that, to date, have shown more evidence in the response and remission of depressive symptoms during the treatment with fluoxetine, citalopram and escitalopram (although there is evidence that the presence of these polymorphisms are also significant in the response to other SSRI and no SSRI antidepressants); These genes are: the 5-HT2A receptor, the 5-HT1A receptor and MAOA.

The serotonin receptor genes 5-HT2A and 5-HT1A regulate the neurotransmission of serotonin in the brain by sequestering serotonine in the synaptic cleft (neuronal chemical connection). Both are important genes in pharmacogenetics of antidepressants since the connection between brain neurons is the main site of action of many families of these drugs. Therefore, determining genetic variants in these genes may lead to a better response to the aforementioned antidepressants.

The MAOA gene (monoamine oxidase A) codes for a protein that degrades certain neurotransmitters, including serotonin (5-HT), therefore the genetic changes in MAOA that predispose to a lower degradation of neurotransmitters has a positive effect on the response to antidepressants.

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