SIMPTOMATIK EPILEPSIYA PATOGENEZIDA FERROPTOZNNING ROLI: KLINIK VA NEYROVIZUALIZATSION TADQIQOT
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simptomatik epilepsiya, ferroptoz, temir almashinuvi, GPX4, kognitiv buzilishlar, neyrovizualizatsiya##article.abstract##
Tadqiqot maqsadi: Simptomatik epilepsiya patogenezida temir almashinuvi buzilishlari va ferroptoz mexanizmlarining rolini o'rganish.
Materiallar va usullar: Simptomatik epilepsiya bilan kasallangan 80 nafar bemor va 30 nafar sog'lom shaxs ishtirokida prospektiv nazoratli kogort tadqiqoti o'tkazildi. Klinik-nevrologik ko'rinishlar, kognitiv funksiyalar (MMSE, TMT), temir almashinuvi ko'rsatkichlari, ferroptoz markerlari (GPX4, ACSL4, MDA), MRT va EEG ma'lumotlari baholandi.
Natijalar: Simptomatik epilepsiyali bemorlarda kognitiv funksiyalarning sezilarli pasayishi (MMSE: 24,3±2,5 vs 28,7±1,3 ball, p<0,01), ferritin darajasining oshishi bilan temir almashinuvi buzilishlari (320±25 vs 210±20 ng/ml, p<0,01), GPX4 ekspressiyasining 1,8 marta kamayishi (p<0,01), ACSL4ning 2,3 marta oshishi (p<0,01) va MDA ning 6,1±0,5 nmol/mg oqsilgacha ko'tarilishi (p<0,001) aniqlandi. SWI-MRT ma'lumotlari bo'yicha bemorlarning 50%ida bazal gangliylar, gippokamp va talamusda temir to'planishi topildi.
Xulosa: Temir almashinuvi buzilishlari va ferroptoz faollashuvi simptomatik epilepsiya patogenezida asosiy rol o'ynaydi, bu patogenetik asoslangan terapiyani ishlab chiqish uchun istiqbollarni ochadi.
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