Hale Gök Dağidir, Duygu Bandirmali, Merve Hilal Ceren Akgör, Doğa Vuralli, Meltem Yalinay, Güvem Gümüş Akay, Hayrunnisa Bolay
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.
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.