Journal Article Epublish
PubMed: 42676989 DOI: 10.55730/1300-0144.6378
Exploratory evaluation of miR-146, inflammatory biomarkers, and subjective cognitive symptoms in chronic migraine.
Turk J Med Sci 56(4):1343-1351
Authors: Hale Gök Dağidir, Duygu Bandirmali, Merve Hilal Ceren Akgör, Doğa Vuralli, Meltem Yalinay, Güvem Gümüş Akay, Hayrunnisa Bolay
Affiliations
- Department of Medical Biochemistry, Faculty of Medicine, Yüksek İhtisas University, Ankara, Turkiye. Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Ankara, Turkiye.
- Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Ankara, Turkiye. Department of Physiology, Faculty of Medicine, Ankara University, Ankara, Turkiye. Brain Research Center (AÜBAUM), Ankara University, Ankara, Turkiye.
- Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Ankara, Turkiye. Department of Neurology and Algology, Faculty of Medicine, Gazi University, Ankara, Turkiye.
- Neuroscience and Neurotechnology Center of Excellence (NÖROM), Gazi University, Ankara, Turkiye.
- Department of Neurology and Algology, Faculty of Medicine, Gazi University, Ankara, Turkiye.
- Neuropsychiatry Center, Gazi University, Ankara, Turkiye.
- Institute of Neuroscience and Neurotechnology, Gazi University, Ankara, Turkiye.
- Department of Clinical Microbiology, Faculty of Medicine, Gazi University, Ankara, Turkiye.
- Department of Physiology, Faculty of Medicine, Ankara University, Ankara, Turkiye.
- Brain Research Center (AÜBAUM), Ankara University, Ankara, Turkiye.
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.
MeSH
Serum, Neurobehavioral Manifestations, Migraine Disorders, Biomarkers, Signs And Symptoms