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The 3′UTR VNTR SLC6A3 Genetic Variant and Major Depressive Disorder: A Systematic Review

Major Depressive Disorder (MDD) is a disabling and particularly persistent mental disorder that is considered to be a priority public health problem. The active human dopamine transporter (DAT), which is encoded by the SLC6A3 gene, regulates the dopamine concentration in the synaptic cleft. In this...

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Detalles Bibliográficos
Autores principales: Gontijo, Bruna Rodrigues, Possatti, Isabella, Fratelli, Caroline Ferreira, Pereira, Alexandre Sampaio Rodrigues, Bonasser, Larissa Sousa Silva, de Souza Silva, Calliandra Maria, Rodrigues da Silva, Izabel Cristina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10452352/
https://www.ncbi.nlm.nih.gov/pubmed/37626766
http://dx.doi.org/10.3390/biomedicines11082270
Descripción
Sumario:Major Depressive Disorder (MDD) is a disabling and particularly persistent mental disorder that is considered to be a priority public health problem. The active human dopamine transporter (DAT), which is encoded by the SLC6A3 gene, regulates the dopamine concentration in the synaptic cleft. In this sense, this neurotransmitter is primordial in modulating human emotions. This systematic review aims to verify the SLC6A3 (DAT1) 3′UTR VNTR (rs28363170) gene variant’s SS (9R/9R) genotype and S (9R) allele frequency fluctuation and its influence on the modulation of pharmacotherapy in MDD. For this purpose, we searched different databases, and after applying the eligibility criteria, six articles were selected. Studies have shown an association between the SS (9R/9R) genotypic and S (9R) allelic presence with the risk of developing MDD, in addition to influencing the decrease in response to antidepressant therapy. However, despite the findings, disagreements were observed between other studies. For this reason, further studies with the SLC6A3 3′UTR VNTR (rs28363170) variant in different populations are necessary to understand this polymorphism’s role in the onset of this disease.