Exploratory evaluation of miR-146, iflamtrnlmaoy biomarkers, and subjective cognitive symptoms in chronic migraine

Abstract

Background/aim: Chronic migraine (CM) is a disabling neurological disorder associated with substantial impairment of quality of life. Increasing evidence suggests that inflammatory and epigenetic mechanisms may contribute to migraine pathophysiology. miR-146, a microRNA involved in the TLR-4/NFkb pathway, is known to regulate proinflammatory signaling, whereas HMGB1 activates inflammatory pathways through TLR2 and TLR4 receptors. IL-17 is another proinflammatory cytokine implicated in both inflammation and cognitive processes. In this research, our aim was to investigate the relationship between serum HMGB1, IL-17, and miR-146 levels and migraine-related subjective cognitive symptoms in patients with CM. Materials and methods: Serum samples were collected from 20 CM patients and 15 age-matched healthy controls. All the participants were female. Medical history, Mini-Mental State Examination (MMSE) scores, and migraine attacks-subjective cognitive impairments scale (Mig-SCog) scores were recorded. Serum HMGB1 and IL-17 levels were measured using an enzyme-linked immunosorbent assay. A quantitative real-time polymerase chain reaction was used to measure serum miR-146 levels. Statistical analysis of the data was conducted with SPSS 25.0. The relationships between Mig-SCog scores and serum HMGB1, IL-17, and miR-146 levels were investigated. Results: Serum HMGB1 levels were significantly elevated in the CM group compared to the control group (p = 0.012). However, no significant differences were observed between the two groups for serum IL-17 (p = 0.737) or miR-146 levels (p = 0.560). There was no significant correlation between HMGB1 and IL-17 (r = 0.167) or HMGB1 and miR146 levels (r = 0.073). Mig-SCog scores (p = 0.001) differed significantly between the groups and were positively correlated with HMGB1 levels (r = 0.403). Conclusion: Serum HMGB1 levels were elevated in CM patients and were associated with migraine-related subjective cognitive complaints, whereas no significant association was observed with miR-146 or IL-17 levels. These findings support a potential role of HMGB1 in migraine-related neuroinflammatory processes. Further studies are needed to clarify the relationship between inflammatory pathways and cognitive symptoms in migraine.