Механизмы появления побочных эффектов и подходы к их ослаблению при лечении неврологических заболеваний
DOI:
https://doi.org/10.33910/2687-1270-2026-7-1-46-76Ключевые слова:
неврологические заболевания, побочные эффекты, нейромодуляторы, базальные ганглии, клауструм, синаптическая пластичностьАннотация
Для неврологических заболеваний характерны изменения состава нейромодуляторов и функционирования нейронных сетей, состоящих из корковых и подкорковых структур. Одна из таких структур — клауструм, реципрокно связанный со многими элементами сети. При системном введении лекарств побочные эффекты становятся результатом нежелательных изменений активности отдельных структур и, следовательно, всей сети. Для ослабления побочных эффектов необходимо понимать механизмы влияния нейромодуляторов на каждую из структур. Дано обоснование сходства механизмов функционирования цепей «кора — базальные ганглии — клауструм — кора» и «кора — базальные ганглии — таламус — кора». Из предложенного нами унифицированного механизма влияния нейромодуляторов на функционирование таких цепей следует, что для улучшения двигательной активности и сенсорного восприятия при лечении болезней Паркинсона и Альцгеймера необходимо повысить активность нейронов таламуса, клауструма и коры, но это может вызвать галлюцинации и бред. Их подавление при лечении психических расстройств может ухудшить двигательную активность. Из механизма следует, что для ослабления побочных эффектов необходимо избирательно воздействовать на рецепторы тех типов, плотность которых в коре невелика. В таком случае ее активность зависит в основном от степени ингибирования со стороны базальных ганглиев нейронов таламуса и клауструма, проецирующихся в кору. С учетом известных данных о расположении рецепторов сделан вывод, что при лечении болезни Паркинсона антагонисты аденозиновых А2А- и серотониновых 5-HT2A-рецепторов могут способствовать ослаблению побочных эффектов леводопы. Антагонисты 5-HT2A-рецепторов в дополнение к типичным антипсихотикам могут ослабить галлюцинации и бред без двигательных нарушений. Этот вывод согласуется с клиническими данными об ослаблении побочных эффектов при использовании антагониста 5-HT2A-рецепторов пимавансерина и антагониста A2A-рецепторов истрадефиллина в дополнение к леводопе, а также атипичного антипсихотика арипипразола, обладающего антагонизмом к 5-HT2A-рецепторам. Предлагаемый подход может быть использован для целенаправленной разработки лекарств, минимизирующих побочные эффекты.
Библиографические ссылки
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