Заключение

Не менее ста лет исследований пролили свет на некоторые механизмы нейродегенерации, сопровождающие БА (Goedert, Spillantini, 2006). В процессе нейродегенерации при БА принимает участие множество молекул и сигнальных путей.

Кальциевая гипотеза БА предполагает, что изменения в кальциевом гомеостазе могут быть как начальным фактором для развития заболевания, так и сопровождать сам процесс нейродегенерации (Emptage et al., 2010; Mattson, 2010; Supnet, Bezpro- zvanny, 2010; Ballard et al., 2011). Однако в рамках этой гипотезы также остается много вопросов: какой кальций-зависимый сигнальный каскад напрямую влияет на патологический процессинг Ap?; какие кальциевые каналы вовлечены в этот процесс?; какие возрастные нарушения регуляции кальциевого гомеостаза в нейронах могут стать ключевыми факторами риска развития БА?; можно ли использовать нарушения кальциевого гомеостаза в клетках в качестве диагностического маркера БА для пожилых людей до развития симптомов?

На данный момент участие кальциевых сигнальных путей в патологии БА показано во многих исследованиях. Фармакологический препарат, модулирующий активность кальциевого канала NMDAR - мемантин - хорошо показал себя в клинических испытаниях и используется в практике лечения БА (Ballard et al., 2011).

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