The Role of Stress-related Biomarkers, Immune-inflammatory Pathways, and Genetic Polymorphisms in Cognitive-behavioral Therapies for Chronic Low Back Pain and Depression: Results from a Randomized Controlled Trial (the IMPACT study).

The Inflammatory Indicator IL-6 and BDNF Levels in Male Fitness Athletes and Their Relationship with Acute Stress Disorder: A Case-Control Study

Neuromolecular biomarkers of traumatic stress: Refining diagnostic criteria and personalizing treatment for core biological symptoms in PTSD.

OBJECTIVE Aim: The aim of this review is to assess the role of neuromolecular biomarkers in post-traumatic stress disorder (PTSD) and their usefulness in improving diagnostic accuracy and supporting personalized treatment strategies. PATIENTS AND METHODS Materials and Methods: A narrative review of studies published between 2015 and 2025 was performed using databases such as PubMed, Scopus, and Web of Science. The analysis included clinical and experimental studies focusing on neuroinflammation, oxidative stress, endoplasmic reticulum stress, and markers of neuronal damage in PTSD. Special attention was given to associations between biomarkers and symptom severity, duration of illness, and treatment outcomes. RESULTS Results: PTSD is associated with disturbances in neuroimmune and neuroendocrine pathways. Increased levels of pro-inflammatory cytokines, including interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18), are frequently observed. Activation of the NLR family pyrin domain containing 3 inflammasome (NLRP3 inflammasome) and elevated oxidative stress markers, such as malondialdehyde (MDA), indicate ongoing inflammatory and oxidative processes. Changes in neuronal injury markers, including ubiquitin carboxyl-terminal hydrolase L1 (UCHL1), suggest neurodegenerative mechanisms. Altered chemokine signaling, particularly fractalkine (chemokine C-X3-C motif ligand 1, CX3CL1), and activation of endoplasmic reticulum stress pathways, such as inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6 (ATF6), are linked to impaired neuronal function and reduced synaptic plasticity. These findings indicate biological heterogeneity within PTSD. CONCLUSION Conclusions: Neuromolecular biomarkers may improve the current symptom-based diagnostic model of PTSD. Their integration with clinical assessment tools may support identification of biologically defined subgroups and enable more targeted treatment.

Innovative Technologies in Social

Neurobehavioral Consequences of Obesity: The Role of Inflammation

Objective Obesity is a global health concern linked to neuroinflammation, cognitive decline, and depression. Tumor necrosis factor-α (TNF-α) is a key mediator of these effects, and its inhibition may offer therapeutic benefits. This study investigated whether etanercept (ETN), a TNF-α inhibitor, prevents neurobehavioral alterations induced by a cafeteria (CAF) diet in rats. Methods Male rats were assigned to control, CAF, or CAF + ETN groups for 12 weeks. Cognitive and affective behaviors were assessed by the Morris water maze, passive avoidance, forced swimming, and sucrose preference tests. Hippocampal TNF-α, interleukin-1β, and brain-derived neurotrophic factor (BDNF) levels were measured. Results CAF-fed rats developed obesity, memory impairment, and depression-like behaviors, accompanied by increased proinflammatory cytokines and reduced BDNF immunoreactivity. ETN attenuated weight gain and improved cognitive and emotional performance with normalized hippocampal proinflammatory cytokines levels. After ETN treatment, BDNF levels significantly increased compared to the CAF group but still remained lower than the controls. Conclusion The results of the study indicate that TNF-α inhibition alleviates obesity-induced neuroinflammation and rescues cognitive and emotional behavioral impairments, while only partially restoring hippocampal BDNF levels. These results suggest a potential link between TNF-α inhibition and the mitigation of obesity-associated neurobehavioral dysfunction through the suppression of hippocampal neuroinflammation.

Depression, Nutritional Status, and Substance P/NK‐1R Biomarkers in Dysmenorrhea: A Randomized Crossover Trial

Substance P (SP) and neurokinin‐1 receptor (NK‐1R) as biomarkers of pain and stress SP and NK‐1R are neuropeptide related biomarkers involved in nociceptive pathways. Dysmenorrhea is frequently associated with psychological distress and biochemical alterations; however, their interrelationship across treatment phases remains insufficiently understood. Objectives To explore changes in psychological status (depression, anxiety, and stress), nutritional status, and SP/NK‐1R‐related biomarker levels across NSAID and dexamethasone plus aprepitant combination therapy phases in females with dysmenorrhea. Methods This was a randomized, sequential, within‐subject repeated‐measures crossover exploratory controlled trial with a parallel healthy control group. A total of 40 females were enrolled, including 30 with primary dysmenorrhea and 10 healthy controls. Dysmenorrhea participants were assessed over three menstrual cycles across three phases: baseline (no treatment), NSAID phase (ibuprofen 400 mg three times daily for 3 days), and combination therapy phase (dexamethasone plus aprepitant for 2 days). Psychological status was assessed using DASS‐21, and nutritional status using the mini nutritional assessment (MNA). Serum SP and NK‐1R levels were measured using ELISA in a subset of participants due to sample limitations. Data were analyzed using IBM SPSS Statistics (version 22), with repeated‐measures ANOVA and independent t‐tests; p  < 0.05 was considered statistically significant. Results Participants with dysmenorrhea were enrolled and assessed for ELISA based SP levels in blood. SP levels showed significant variation across treatment phases (p = 0.021), with the lowest values observed during the dexamethasone plus aprepitant phase compared to baseline and NSAID phases. NK‐1R levels did not show significant phase‐wise changes. Psychological subgroup analyses indicated greater SP variability in participants with moderate depression, stress, and anxiety, although several subgroups were small. Nutritional status showed partial associations with SP changes, with significant differences in malnourished and normal groups. Overall, biomarker changes were more pronounced than NK‐1R alterations across phases. Conclusion This study demonstrates phase‐dependent changes in SP levels alongside psychological and nutritional variations in women with dysmenorrhea. However, absence of clinical pain outcomes and small subgroup sizes limit causal interpretation, and findings should be considered preliminary and biomarker‐focused.

Relationships of oxidative stress, inflammation and gut microbiota with cognitive impairment in first-episode major depressive disorders: a pilot study in China

The research showed that the GM and their predicted metabolic pathways in patients with MDD were closely related to cognitive function and peripheral blood indicators, and that differences in these factors may manifest as oxidative stress and inflammation.