Журнал высшей нервной деятельности им. И.П. Павлова, 2023, T. 73, № 4, стр. 454-478

Нейровоспаление и иммунные нарушения в механизмах развития болезни Паркинсона

Г. В. Идова 1*, Е. Л. Альперина 1, С. Я. Жанаева 1

1 Федеральное государственное бюджетное научное учреждение “Научно-исследовательский институт нейронаук и медицины”
Новосибирск, Россия

* E-mail: galina-idova@mail.ru

Поступила в редакцию 26.12.2022
После доработки 25.02.2023
Принята к публикации 27.02.2023

Аннотация

Болезнь Паркинсона (БП) – хроническое прогрессирующее нейродегенеративное расстройство, проявляющееся гибелью дофаминовых нейронов, агрегацией α-синуклеина и выраженными моторными нарушениями. В обзоре рассматриваются современные данные о ключевой роли нейровоспаления и иммунной дисфункции в нейродегенерации и развитии заболевания. Приведены клинические и экспериментальные доказательства активации микроглии, участия в этом процессе Toлл-подобных рецепторов, широкого спектра хемокинов и про- и противовоспалительных цитокинов в динамике течения заболевания. Особое внимание уделено роли врожденного и адаптивного иммунного ответа в механизмах системного воспаления в мозге и на периферии. Продемонстрировано включение в процесс нейровоспаления и нейродегенерации инфильтрирующих мозг иммунных клеток и их субпопуляций, изменение состава и фенотипа периферических иммунных клеток и их функциональных характеристик. Анализ подмножеств иммунных клеток и их соотношения позволяет выявить тонкие, специфичные для БП, изменения в клеточных популяциях, которые могут быть использованы в качестве надежных биомаркеров для диагностики, прогнозирования течения заболевания и разработки новых подходов к противовоспалительной и таргетной терапии БП.

Ключевые слова: болезнь Паркинсона, дофамин, α-синуклеин, нейровоспаление, микроглия, Толл-подобные рецепторы, хемокины, про- и противовоспалительные цитокины, моноциты, субпопуляции Т- и В-клеток

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