Аннотация
Предполагается, что бета-амилоидный пептид (Аβ-пептид) играет центральную роль в возникновении болезни Альцгеймера (БА). Эта патология связана с быстрым накоплением нейротоксичных амилоидных агрегатов в тканях мозга, хотя основы прогрессирования заболевания остаются неразрешенными. Отмечено, что доклиническая стадия БА может играть решающую роль в дальнейшем необратимом развитии болезни. В частности, взаимодействия между липидными мембранами и молекулами Аβ-пептида, встроенного в мембрану в относительно низких концентрациях, должны находиться под пристальным вниманием исследователей. В этом обзоре мы обсуждаем недавние работы, посвященные изучению липид-пептидных взаимодействий, с акцентом на вызванную пептидом Аβ(25-35) реорганизацию липидных мембран в условиях, имитирующих доклиническую стадию БА. Предполагается, что наблюдаемые взаимодействия важны для понимания механизмов деструктивного воздействия Аβ-пептида на липидные мембраны и последующего возникновения заболевания. Методы прикладной ядерной физики оказались чрезвычайно актуальными в таких исследованиях. Методы рассеяния предоставили инструментальную информацию на уровне надмолекулярных агрегатов, в то время как спектроскопия позволила получить информацию на молекулярном уровне. Наконец, компьютерное моделирование методом молекулярной динамики предоставило детали, недостижимые экспериментальными подходами, хотя в ключевой роли последних невозможно усомниться. Таким образом, последние достижения в исследованиях доказывают, что эти взаимодополняющие подходы являются наиболее подходящими для решения сложных проблем во взаимодействиях биомембран.
Поддерживающие организации
Библиографические ссылки
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