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BIN1 (амфифизин 2) в патогенезе когнитивных нарушений

BIN1 (амфифизин 2) в патогенезе когнитивных нарушений

Авторы:
Инна Юрьевна Шамакина,
Виктор Сергеевич Кохан,
Валерия Алексеевна Венкова,
Валерия Юрьевна Баронец,
Севастьян Степанович Попов,
Петр Константинович Анохин

Журнал: Журнал неврологии и психиатрии им. С.С. Корсакова. 2026;126(3):45-52.

DOI: 10.17116/jnevro202612603145

Прочитано: 849 раз

Резюме

Как показал полногеномный поиск ассоциаций (GWAS), ген мостикового интегратора 1 (Bridging integrator 1, BIN1) — второй по значимости после аполипопротеина E (APOE) генетический локус, ассоциированный с риском болезни Альцгеймера (БА). Кодируемый этим геном амфифизин 2 (Bin1) представляет собой адаптерный белок, участвующий в регуляции синаптического везикулярного транспорта и нейротрансмиссии. Установлено, что у пациентов с БА уровень экспрессии белка Bin1 изменен в нескольких областях мозга, включая гиппокамп, что может влиять на тау-зависимую нейропатологию и прогрессирование заболевания. В настоящем обзоре представлены современные данные о структуре, функциях и потенциальной роли Bin1 в патогенезе когнитивных нарушений различной степени тяжести и возможности использования аллельного полиморфизма гена BIN1 в диагностике когнитивных нарушений и риска БА.

Ключевые слова

  • BIN1
  • когнитивные нарушения
  • болезнь Альцгеймера
  • тау-белок
  • полиморфизм генов
  • аллель риска

Дата поступления: 01.08.2025

Дата принятия в печать: 31.08.2025

Дата публикации: 15.04.2026

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