Заключение

На основании анализа большого блока экспериментальных и клинических исследований мы представили описание начальных этапов физико-биохимических событий в нейронах, которые являются пусковыми факторами развития амилои- доза нейронов и раннего патогенеза БА.

Подводя итоги можно констатировать, что процесс образования межклеточных бляшек, фибрилл и волокон является приспособительной реакцией организма для сохранения функциональной активности основных рефлекторных процессов при утрате биохимических межнейрональных контактов. Исследование мощной экспериментальной базы позволило выявить значительные изменения нейробиологического каскада в нейронах при начальном развитии амилоидоза нейронов в латентной стадии БА, которые вызывают вторичные внутринейрональные изменения метаболического и структурного характера и демонстрируют мультифакторность патологического процесса. Мы согласны с мнением большинства исследователей, что для определения начальных этапов амилоидоза нейронов и диагностики латентной стадии БА наиболее надежными маркерами являются Ар (Masliah et al., 1996; Niedowicz et al., 2012) с физиологической конформацией и конформационно модифицированные нано-Ар, а также гиперфосфорилированный ТБ (Braak, Braak, 1996; Chun, Johnson, 2007b).

Наши выводы убедительно показывают, что все вышеописанные процессы протекают параллельно. При этом нейроны максимально используют все защитные ресурсы клетки, чтобы избежать гибели. Полученные результаты предлагают новые подходы к разработке молекулярной диагностики БА и открывают новые перспективы поиска оптимальной патогенетической терапии БА.

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