The aim of this study was to elucidate the clinical picture of Major Depressive Disorder (MDD) with polymorphisms involving the IL6 gene. It was a systematic review with a search for original articles in the Scopus, Web of Science, PubMed, and BVS databases, which provided information on genetic variants related to IL6 gene polymorphisms. Studies that did not present complete data, including statistical data, were excluded. Fifty-four articles were found in the databases. The Rayyan platform was used to remove duplicates and read abstracts for initial selection. Twelve articles remained, and those that were freely accessible were selected for full reading, totaling 5 articles for this review. Evidence suggests a systemic condition in MDD, with data demonstrating inflammatory alterations. Given that in most studies, patients with MDD had higher inflammatory states, there appears to be a relationship between IL-6 and the disorder. IL-6 induces changes in the brain, activates microglia, and controls neuronal health, potentially making the relationship between polymorphisms and the disease tangible, but there are still few studies in the field.

Introduction: Major Depressive Disorder (MDD) has been increasingly associated with inflammatory dysregulation, particularly involving tumor necrosis factor-alpha (TNF-α). Genetic polymorphisms within the TNFA promoter region have been investigated as potential modulators of depressive susceptibility, symptom expression, treatment response, and inflammatory comorbidity. However, findings remain inconsistent across populations and clinical contexts. Methods: This systematic review adhered to PRISMA 2020 guidelines and was registered in PROSPERO (CRD420251242724). Observational and interventional studies evaluating associations between TNFA polymorphisms—specifically rs1800629 (−308 G/A), rs1799724 (−857 C/T), and rs1799964 (−1031 T/C)—and MDD-related outcomes in adults were included. Data extraction and methodological quality assessment were performed independently using an adapted GRIPS framework. Results: Eleven studies met the inclusion criteria, with eight investigating MDD without cardiovascular comorbidity and three assessing cardiovascular populations. Across diverse cohorts, rs1800629 and rs1799724 did not demonstrate consistent associations with MDD susceptibility. Although isolated population-specific findings were reported, genotype and allele distributions were generally comparable between cases and controls. Rs1799724 was associated with symptom dimensions and altered TNF-α expression in two cohorts. Rs1799964 was not linked to disease occurrence but showed potential association with antidepressant response and adverse cardiovascular outcomes in patients with chronic heart failure and comorbid depression. Overall, findings were heterogeneous and influenced by population characteristics, sample size, and clinical context. Conclusions: Current evidence does not support a robust etiological role for TNFA promoter polymorphisms in major depressive disorder. These variants may exert context-dependent modulatory effects on symptom expression, treatment response, or inflammatory-cardiovascular interactions rather than serving as primary susceptibility determinants. Larger, ethnically diverse studies integrating genetic, inflammatory, and clinical data are required to clarify the contribution of inflammatory genetic variability in depressive disorders.

Introduction: Stroke remains a leading cause of morbidity and mortality in Brazil, requiring rapid and effective responses from the initial point of care

Introduction: Lipid metabolism disturbances have been linked to depression pathophysiology, with apolipoprotein B (APOB)—a key component of LDL particles—emerging as a relevant biomarker

Major Depressive Disorder (MDD) is strongly associated with suicidal behavior

The aim of this study was to assess whether biochemical, biological, and anthropometric characteristics are related to the XbaI polymorphism of APOB in obese patients aged 50+, as well as to verify susceptibility to health impairment. This research is a cross-sectional, comparative, analytical study with both quantitative and qualitative approaches, consisting of 21 elderly women aged 50 years or older who underwent Roux-en-Y- gastric bypass surgery one year ago. Clinical data and blood samples were collected 12 months after surgery, and genotyping was performed using the PCR-RFLP technique. The data indicated that there was no statistical association between the presence of the polymorphism and morbid obesity (P=0,302); however, it was found that the X+ alelle leads to reduced median of adipose mass in patients (P=0,031).