Эпигенетика, генетика и биохимия суицидов

Автор: Козлов В.А., Голенков А.В., Орлов Ф.В.

Статья в выпуске: 3 (52) т.14, 2023 года.

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Развитие методов молекулярной биологии позволило выявить новые, ранее неизвестные механизмы формирования суицидального фенотипа и суицидального поведения. Специалистам в области суицидологии это позволило расценить суицидальный фенотип как самостоятельную полигенную и мультифакторную патологию, которая может сопутствовать психическим заболеваниям как коморбидное состояние. Цель публикации - систематизация известных данных литературы о стойких биохимических изменениях, ассоциируемых с суицидальным фенотипом. Рассмотрены эпигенетические, генетические и биохимические маркеры, ассоциированные с суицидальным поведением и суицидами лиц без предшествующих психических заболеваний, а также молекулярно-биологический анализ случаев суицида у больных с большим депрессивным расстройством. Анализ современной литературы - публикации прямых исследований биологического материала, полученных от лиц с суицидальным поведением и суицидентов, а также метаанализов - даёт основания считать базовой причиной суицидального фенотипа нейровоспаление и/или проникновение в ликворную жидкость через генуинно скомпрометированный гематоэнцефалический барьер воспалительных цитокинов, образующихся у лиц с длительно протекающими истощающими хроническими воспалительными заболеваниями (латентная инфекция Toxoplasma gondii, ревматоидные заболевания, атопический дерматит, бронхиальная астма). Нейровоспаление, формирующее суицидальный фенотип, реализуется в результате однонуклеотидных полиморфизмов генов, ассоцииро ванных с генами гомеобокса и иммунного ответа, таких как интерлейкины-2, -4, -6, фактор некроза опухоли. В то время как интерлейкин-8, возможно оказывает защитный эффект. Кроме того, суицидальный фенотип с большой долей вероятности связан с генетически обусловленным нарушением обмена триптофана, вызванным активацией кинуренинового пути с сопутствующим истощением пула серотонина и индуцированием нейровоспаления по кинурениновому типу. Хроническое нейровоспаление меняет психотип и поведение в сторону формирования суицидального фенотипа. В результате индивидуум формирует вокруг себя социальную среду, способствующую отягчению нейровоспаления, и суициду как финалу заболевания. Сделан вывод, что суицидальный фенотип формируется нейровоспалением.

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Суицид, однонуклеотидные полиморфизмы, эпигенетика, генетика биохимия, нейровоспаление, кинуренин, toxoplasma gondii, кетамин, соли лития, холекальциферол

Короткий адрес: https://sciup.org/140301926

IDR: 140301926 | DOI: 10.32878/suiciderus.23-14-03(52)-27-50

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