Заключение
В заключение этой главы следует подчеркнуть, что понимание молекулярных механизмов патогенеза БА, и в частности метаболизма, предшественника амилоидного пептида, позволяет расширить сложившиеся на сегодняшний день представления о причинах возникновения этого нейродегенеративного заболевания, на развитие которого влияют многочисленные внешние и внутренние факторы и в патогенез которого вовлечены множественные метаболические процессы (рис.
7). Их углубленное изучение открывает новые терапевтические направления коррекции биохимических процессов, нарушенные в ходе развития и жизнедеятельности организма и приводящие к развитию патологии. В данном контексте важно отметить, что направленная регуляция экспрессии и активности амилоид-деградирую- щих ферментов может быть оправданным и недорогим способом профилактики БА. В частности, даже незначительное одновременное повышение активности нескольких амилоид-деградирующих ферментов может препятствовать накоплению токсических концентраций амилоидного пептида и предотвращать запуск каскада патологических реакций, ведущих к нейропатологии и БА.
Рис. 7. Схематическое изображение каскада патологических изменений, имеющих место при нейродегенерации и БА, и факторов, влияющих на их развитие
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