Major Depressive Disorder (MDD) is a disease that involves biological, psychological, and social interactions. Studies have shown the importance of genetics contribution to MDD development. The SCL6A4 protein (5HTTLPR) functions transporting serotonin, a neurotransmitter linked to mood and emotion, to the synaptic cleft. Hence, this study seeks, through a literature review, a better comprehension of the 5HTTLPR genetic variant association with MDD. For this purpose, a search was performed on the Virtual Health Library Portal for articles that related 5HTTLPR to MDD. Most of the articles found were conducted in the American continent, with one (1) study implemented in Brazil. 5HTTLPR associations were found regarding changes in the nervous system, pharmacology, and risk factors seen in MDD patients. When verifying the allelic distribution, the S allele had a higher frequency in most of the studies analyzed. Despite not finding a commonality in the different studies, the tremendous genetic variation found demonstrates the MDD complexity. For this reason, further studies in diverse populations should be conducted to assist in the understanding and treatment of the disease.

Major depressive disorder (MDD) still has an unknown etiology and mechanisms. Many studies have been conducted seeking to associate and understand the connection of different genetic variants to this disease. Researchers have extensively studied the brain-derived neurotrophic factor (BDNF) Val66Met genetic variant in MDD; yet, their findings remain inconsistent. This systematic review sought to verify the GG (Val/Val) genotype frequency fluctuation in different populations with MDD. For this, we searched in different databases and, after applying the eligibility criteria, selected 17 articles. Most studies demonstrate the higher frequency of the ancestral (wild) GG (Val/Val) genotype, although associations of the polymorphic A (Met) allele, changes in BDNF protein serum levels, or both were also found in MDD, whether related to the disease’s development or other factors. Nevertheless, despite these findings, disagreements between several studies are seen. For this reason, further BDNF Val66Met genetic variant studies should not only bridge the gap in the knowledge of this polymorphism’s role in MDD’s different facets but also analyze the genotypic and phenotypic heterogeneity in different populations to help provide a better quality of life for patients.

Major Depressive Disorder (MDD) is a highly prevalent multifactorial psychopathology affected by neurotransmitter levels. Monoamine Oxidase A (MAOA) influences several neural pathways by modulating these levels. This systematic review (per PRISMA protocol and PECOS strategy) endeavors to understand the MAOA uVNTR polymorphism influence on MDD and evaluate its 3R/3R and 3R* genotypic frequencies fluctuation in MDD patients from different populations. We searched the Web of Science, PubMed, Virtual Health Library, and EMBASE databases for eligible original articles that brought data on genotypic frequencies related to the MAOA uVNTR variant in patients with MDD. We excluded studies with incomplete data (including statistical data), reviews, meta-analyses, and abstracts. Initially, we found 43 articles. After removing duplicates and applying the inclusion/exclusion criteria, seven articles remained. The population samples studied were predominantly Asians, with high 3R and 4R allele frequencies. Notably, we observed higher 3R/3R (female) and 3R* (male) genotype frequencies in the healthy control groups and higher 4R/4R (female) and 4R* (male) genotype frequencies in the MDD groups in the majority of different populations. Despite some similarities in the articles analyzed, there is still no consensus on the MAOA uVNTR variant’s role in MDD pathogenesis.