Background: There are studies that have investigated the association of pro-inflammatory cytokines with depressive disorders, but they often present certain limitations. In this study, two substantial groups of patients were analyzed: 92 patients with major depressive disorder and 76 without depressive disorders. The strict inclusion and exclusion criteria for the analyzed groups significantly increased the value of the obtained results. The research question of this study was whether levels of inflammation, measured by the inflammatory markers IL-6, IL-1α, and TNF-α, could predict the severity of depressive symptoms. This could provide additional evidence supporting the hypothesis that inflammation plays a notable role in the pathogenesis of depression. The data analysis supports the hypothesis that the biological mechanisms of inflammation contribute to the clinical manifestations of depression. Elevated levels of inflammatory markers, especially interleukins (IL-6, IL-1α) and tumor necrosis factor-alpha (TNF α), have been identified in patients with major depressive disorder compared to the findings in healthy controls. Materials and Methods: Inflammatory markers (IL-6, IL-1α, and TNF-α) were measured in a sample of 92 patients hospitalized at the Socola Institute of Psychiatry in Iasi, Romania, and compared to a control group with no depression or inflammatory conditions (n = 76). Severity of depressive symptoms was assessed using HAM-D scores. Results: The study results indicated that values of plasma inflammatory markers were significantly higher in patients with major depressive disorder (MDD) compared to the control group (IL-1α: 1.16 ± 0.44 pg/mL vs. 0.89 ± 0.25 pg/mL, p = 0.0004; IL-6: 9.21 ± 4.82 pg/mL vs. 7.16 ± 4.32 pg/mL, p = 0.0149; and TNF-α: 2.02 ± 0.96 pg/mL vs. 1.67 ± 0.8 pg/mL, p = 0.0286). The differences remained significant after applying logarithmic transformation, which was necessary to adjust for outlier values. An analysis of demographic characteristics showed that the frequency of women (67.4% vs. 36.84%, p < 0.001), cohabiting individuals (28.26% vs. 10.53%, p = 0.0001), and alcohol consumers (67.39% vs. 47.37%, p = 0.0087) was significantly higher in patients with MDD. The level of education was significantly lower in patients with MDD (median (IQR): 12 (2.5) years vs. 14 (8) years, p = 0.0016). The evaluation of confounding variables, including patients’ gender, marital status, education level, and alcohol consumption, was performed using multiple linear regression models. The results indicated that these demographic variables did not significantly influence the correlation between the HAM-D score and the values of IL-6, IL-1α, and TNF-α. A significant correlation between the HAM-D score and the logarithmic values of inflammatory markers was observed for log IL-1α in men (r = 0.355, p = 0.0014), log IL-6 in women (r = 0.0313, p = 0.0027), and log TNF-α in women (r = 0.3922, p = 0.0001). The results of the multiple linear regression and predictive analysis indicated that IL-1α (AUC = 0.677, p = 0.0004), IL-6 (AUC = 0.724, p < 0.001), and TNF-α (AUC = 0.861, p < 0.001) demonstrate high accuracy in discriminating patients with MDD. Conclusions: The results highlighted that IL-6 (AUC = 0.724; 95% CI: 0.648–0.801) and TNF-α (AUC = 0.861; 95% CI: 0.797–0.925) are significant predictors for major depressive disorder. The study highlights the potential of cytokines (IL-1α, IL-6 and TNF-α) as diagnostic markers. These findings support the hypothesis that inflammation may play an important role in the development or exacerbation of depressive symptoms.

Background/Objectives: Kidney transplantation remains the gold standard treatment of end-stage kidney disease; however, its recipients exhibit mixed clinical trajectories, with variable renal function and proteinuria evolution over time. Currently used methods to screen these changes are associated with possible adverse effects and limitations. Methods: In this single-center cohort study, 174 adult kidney transplant recipients were enrolled between January 2024 and January 2025 and followed for 12 months. Patients underwent serum and urinary metabolomic profiling using nuclear magnetic resonance (NMR) spectroscopy. Furthermore, clinical and biological data were collected, allowing for assessment of changes in renal function and proteinuria, with patient stratification based on outcome trends. Results: Serum metabolomic profiles were linked to renal outcomes. For ΔeGFR, valine differed between patients with positive and negative trajectories, while GlycA, GlycB and Glyc/SPC were associated with ΔeGFR in adjusted models. For Δproteinuria, GlycA, VLDL particles and triglycerides showed correlations, while glucose differed between patients with improving and worsening proteinuria. In adjusted models, isoleucine, alanine, GlycA and Glyc/SPC were associated with Δproteinuria. Urinary metabolomic profiles showed fewer associations. Dimethylamine and urinary creatinine were associated with ΔeGFR in adjusted models, while acetic acid differed between proteinuria groups. No urinary metabolite was associated with Δproteinuria after adjustment. Conclusions: Overall, metabolomic changes were connected with renal outcomes in kidney transplant patients, with distinct but partially overlapping patterns for ΔGFR and Δproteinuria. Serum findings were more consistent, while urinary associations were more limited. Further longitudinal and externally validated studies are required to confirm these observations and explore the potential of this metabolomic approach in the search for novel biomarkers.

With the burden of dementia growing worldwide and its increasing prevalence, there is an urgent need for treatments that can effectively target the main mechanisms of the neurodegenerative process [1]. A lot of hope lies in traditional herbal medicine, particulary Ginkgo Biloba, wich is believed to not only stop the neurodegenerative process, but also to alleviate the neuropsychiatric symptoms of dementia [2]. However, current literature tends to overlook the demographic-specific effects of Ginkgo Biloba, not clarifying the efficacy across varied patient profiles. In this context, we conducted a thorough search across multiple databases, focusing on Ginkgo Biloba impact age, sex, genetic phenotype and type of dementia. Our conclusions reaveled a varied efficacy between different demographic groups, with noticeable benefits in some populations or even fewer adverse effects in others. Particularly, we identified that groups with older adults and specific genetic markers exhibited the most significant improvements in cognition, signifying that there is a strong need for personalized therapeutic strategies, using the demographic considerations in clinical decision making. This review aims to highlight the benefits of herbal medicine, principally Ginkgo Biloba, in adapted dementia care, even though deeper research is needed to develop accurate treatment protocols for assorted patient populations.

The primary objective of this study is to determine the existence of a significant correlation between inflammation levels, as measured by inflammatory markers IL-6, IL-1β, and TNF-α, and the severity of depressive symptoms assessed using HAM-D assessment scale. This could provide additional evidence supporting the hypothesis that inflammation plays a notable role in the pathogenesis of depression. The data analysis supports the hypothesis that the biological mechanisms of inflammation contributes to the clinical manifestations of depression. Elevated levels of inflammatory markers, especially interleukins (IL6, IL1β), tumor necrosis factor-alpha (TNFα), and C-reactive protein (CRP) have been identified in patients with major depressive disorder compared to the findings in healthy controls. Materials and Methods: Inflammatory markers (IL-6, IL-1β, and TNF-α) were measured in a sample of 31 patients hospitalized at the Socola Institute of Psychiatry in Iasi, Romania, and compared to a control group with no psychiatric or inflammatory conditions. One of the main objectives is to determine if there is a significant correlation between inflammation levels, measured by inflammatory markers (IL-6, IL-1β, and TNF-α), and the severity of depressive symptoms assessed using HAM-D scores. Conclusions: The study results suggest a significant correlation between inflammation levels measured by inflammatory markers IL-1β and IL-6 and the severity of depressive symptoms evaluated by HAM-D scores in the study group. These findings support the hypothesis that inflammation may play an important role in the development or exacerbation of depressive symptoms. The relationship between inflammation and depression is also influenced by risk and protective factors that require further research.