Objectives: Obsessive-compulsive disorder (OCD) is a neuropsychiatric disorder characterized by obsessions and compulsions, with a prevalence of 1%–3%. Tight junction (TJ) proteins contribute to maintaining the epithelial barrier. This study investigated the association of serum TJ-associated MARVEL protein family and inflammatory markers with OCD severity in children and adolescents. Methods: A total of 43 drug-naive children with “pure” OCD and 37 age-matched healthy controls were included in the study. Serum levels of occludin, tricellulin, MarvelD3, which belong to the TJ-associated MARVEL protein family, along with inflammatory markers (C-reactive protein, tumor necrosis factor-alpha [TNF-α], interleukin-6) were assessed. The severity of OCD was ascertained using the Maudsley Obsessive-Compulsive Inventory (MOCI). Biochemical data of patients and control groups were compared against clinical features such as OCD severity and time since symptom onset. Results: Both groups showed similar sociodemographic factors, except that psychiatric disorders and family histories of OCD were significantly higher in the OCD group. Although serum TJ levels were not significantly different between groups, serum tricellulin (r= 0.427, p=0.004), MarvelD3 (r=0.489, p<0.001), and TNF-α (r=0.495, p<0.001) levels had a positive correlation with the severity of OCD based on MOCI. Conclusion The findings suggest that tricellulin, MarvelD3, and TNF-α may be associated with OCD severity. Further comprehensive research is required to determine the role of TJ proteins belonging to the MARVEL protein family in the pathophysiology of OCD.

Objective: ADHD, a prevalent neurodevelopmental disorder affecting 5−7% of children and adolescents, is characterized by inattention, hyperactivity, and impulsivity, impacting social and academic functioning. Its complex etiology includes genetic, environmental, and inflammatory factors. In the present research, we aimed to compare serum CRP, TNF-α, IL-6, IFN-γ, TWEAK, neopterin and zinc levels in drug-naive ADHD patients and healthy controls. Methods: This study included 50 drug-naïve ADHD patients (aged 8−18) and 37 healthy controls. Psychiatric diagnoses were based on DSM-5 criteria. Blood samples were analyzed for inflammatory markers, including CRP, TNF-α, IL-6, IFN-γ, TWEAK, neopterin, and zinc. Statistical analyses were performed using SPSS. Results: The study found no significant differences in age, sex, or BMI between individuals with ADHD and the control group. Regarding inflammatory markers, ADHD patients demonstrated significantly lower levels of TWEAK and higher levels of CRP compared to controls. However, no differences were observed in the levels of TNF-α, IL-6, IFN-γ, zinc, or neopterin. When examining ADHD subtypes, it was noted that individuals with the inattentive subtype had markedly lower TWEAK levels and higher CRP levels than the control group. Conclusion This finding particularly supports that TWEAK levels could be a significant marker both for ADHD and the predominantly inattentive subtype. Additionally, a correlation was identified between IFN-γ levels and psychosomatic symptoms, and this positive correlation suggests that this cytokine may be associated with specific ADHD symptoms. This study highlights the role of neuroinflammatory processes in ADHD and the etiological distinction of the predominantly inattentive ADHD subtype from other subtypes in the literature. Future research should validate these findings through larger and longitudinal studies.