Заключение

В настоящее время участие а-синуклеина в патогенезе БП подтверждается в ряде исследований. Разработка диагностических тестов БП основанных на оценке

Рис.

уровня а-синуклеина в различных тканях человека остается, однако, задачей нерешенной. Отсутствие такихтестов обусловлено, в первую очередь, отсутствием ясного понимания того, какие агрегаты а-синуклеина обладают нейротоксичностью, а также сложностью разработки методов специфичного выявления олигомерных нейротоксичныхформ а-синуклеина и их дифференцировки от физиологически активных тетрамеров белка. Анализ литературных данных, а также результаты собственных исследований предполагают, что оценка уровня немодифицированного как общего, так и олигомерного а-синуклеина крови сегодня не может быть использована в качестве прогностического маркера БП. Результаты остаются противоречивыми даже при учете фактора гемолиза и обследовании групп пациентов, не принимающих препараты Л-ДОФА. Альтернативно, перспективным представляется измерение модифицированных форм а-синуклеина в крови, а также оценка а-синуклеина в клеточных фракциях крови, полученных путем клеточного сортин- га, в частности в CD45+ клеточных лизатах. Формирование агрегатов а-синуклеина при других заболеваниях человека указывает на необходимость адекватной оценки специфичности предлагаемых маркеров. Наиболее прогностически значимым может стать развитие методов нейровизуализации, способных выявлять накопление а-синуклеина в отделах мозга.

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