| Autor: |
CHERKEZZADE, Minara, SOYLU, Selen, TÜZÜN, Erdem, YILMAZ, Vuslat, SEZGİN, Mine, YAPICI, Zuhal, KÜÇÜKALİ, Cem İsmail, TOPALOĞLU, Pınar |
| Předmět: |
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| Zdroj: |
Archives of Neuropsychiatry / Nöropsikiyatri Arşivi; Jun2024, Vol. 61 Issue 2, p128-134, 7p |
| Abstrakt: |
Introduction: Although the contribution of enhanced glial activity in seizure induction is increasingly recognized, the role of glia-induced neuroinflammation in the physiopathology of epileptic encephalopathy (EE) has been scarcely investigated. Methods: To delineate the contribution of glial activity in EE, we measured levels of glia-derived mediators with previously described biomarker value, including glial fibrillary acidic protein (GFAP), high mobility group box 1 (HMGB1), chitinase-3-like protein 1 (CHI3L1), soluble CD163 (sCD163) and triggering receptor expressed on myeloid cells 2 (TREM2) by ELISA in sera of patients with idiopathic West syndrome (WS, n=18), idiopathic Lennox-Gastaut syndrome (LGS, n=13) and healthy controls (n=31). Results: Patients with EE showed significantly higher CHI3L1 levels compared to healthy controls. Levels of HMGB1, CHI3L1, sCD163 and TREM2 were higher in LGS patients than WS patients and/or healthy controls. One or more of the investigated mediators were associated with treatment responsiveness, disease severity and presence of pathological features on electroencephalography (EEG). Conclusions: To our knowledge, our findings provide the initial patient-based evidence that astrocyte- and microglia-mediated neuroinflammation might be involved in the pathogenesis of LGS and WS. Moreover, glial mediators may serve as prognostic biomarkers in patients with idiopathic EE. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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