psychiatryПСИХИАТРИЯPsychiatry (Moscow) (Psikhiatriya)1683-83192618-6667FSBSI “The Mental Health Research Centre”; LLC «Publisher «MIA»10.30629/2618-6667-2023-21-6-85-99psychiatry-1071Research ArticleНАУЧНЫЕ ОБЗОРЫSCIENTIFIC REVIEWSОкислительный стресс при шизофрении: связь с нейрохимическими патогенетическими гипотезамиOxidative Stress in Schizophrenia: Relation to Neurochemical Pathogenetic Hypotheseshttps://orcid.org/0000-0001-7744-533XБурбаеваГ. Ш.BurbaevaG. Sh.

Гульнур Шингожиевна Бурбаева, доктор биологических наук, профессор, заведующая лабораторией

лаборатория нейрохимии

Москва

Gulnur Sh. Burbaeva, Dr. of Sci. (Biol.), Professor, Head of the Laboratory

Laboratory of Neurochemistry

Moscow

gburb@mail.ruhttps://orcid.org/0000-0002-3574-2165ПрохороваТ. А.ProkhorovaT. A.

Татьяна Андреевна Прохорова, научный сотрудник

лаборатория нейрохимии

Москва

Tatyana A. Prokhorova, Researcher

Laboratory of Neurochemistry

Moscow

gnidra@mail.ruhttps://orcid.org/0000-0002-5996-6606СавушкинаО. К.SavushkinaO. K.

Ольга Константиновна Савушкина, кандидат биологических наук, ведущий научный сотрудник

лаборатория нейрохимии

Москва

Olga K. Savushkina, Cand. of Sci. (Biol.), Leading Researcher

Laboratory of Neurochemistry

Moscow

osavushkina1@yandex.ruhttps://orcid.org/0000-0002-4784-8995ТерешкинаЕ. Б.TereshkinaE. B.

Елена Борисовна Терешкина, кандидат биологических наук, старший научный сотрудник

лаборатория нейрохимии

Москва

Elena B. Tereshkina, Cand. of Sci. (Biol.), Senior Researcher

Laboratory of Neurochemistry

Moscow

tereshkina.el@yandex.ruhttps://orcid.org/0000-0002-5766-0910ВоробьеваЕ. А.VorobyevaE. A.

Елена Анатольевна Воробьева, кандидат биологических наук, научный сотрудник

лаборатория нейрохимии

Москва

Elena A. Vorobyeva, Cand. of Sci. (Biol.), Researcher

Laboratory of Neurochemistry

Moscow

vaa-vea-@yandex.ruhttps://orcid.org/0000-0003-1369-8658БокшаИ. С.BokshaI. S.

Ирина Сергеевна Бокша, доктор биологических наук, главный научный сотрудник

лаборатория нейрохимии

Москва

Irina S. Boksha, Dr. of Sci. (Biol.), Chief Scientific Researcher

Laboratory of Neurochemistry

Moscow

boksha_irina@mail.ruФГБНУ «Научный центр психического здоровья»РоссияFSBSI “Mental Health Research Centre”Russian Federation2023040120242168599Copyright © Бурбаева Г.Ш., Прохорова Т.А., Савушкина О.К., Терешкина Е.Б., Воробьева Е.А., Бокша И.С., 20242024Бурбаева Г.Ш., Прохорова Т.А., Савушкина О.К., Терешкина Е.Б., Воробьева Е.А., Бокша И.С.Burbaeva G.S., Prokhorova T.A., Savushkina O.K., Tereshkina E.B., Vorobyeva E.A., Boksha I.S.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.journalpsychiatry.com/jour/article/view/1071   Обоснование

   Обоснование: гетерогенность шизофрении отражается в разнообразии клинических проявлений и биологических нарушений, изучение которых послужило основой для выдвижения нейрохимических гипотез патогенеза шизофрении. Обзор современных гипотез патогенеза шизофрении показывает, что окислительный стресс не является основной причиной развития заболевания, но влияет на его течение и вносит вклад в ухудшение состояния больного.

   Цель

   Цель: проанализировать связь нарушений окислительно-восстановительного баланса и окислительного стресса с развитием патологических процессов при шизофрении в рамках нейрохимических гипотез патогенеза заболевания.

   Материалы и методы

   Материалы и методы: по сочетаниям ключевых слов «окислительный стресс», «окислительно-восстановительный дисбаланс», «шизофрения», «гипотезы патогенеза шизофрении», «антиоксиданты», «нейромедиаторы», «глутатион», «нейровоспаление» проведен поиск источников по базам данных Medline/PubMed, Scopus и РИНЦ.

   Заключение

   Заключение: данные многочисленных исследований головного мозга больных шизофренией, плазмы и сыворотки крови, форменных элементов крови и изучение моделей шизофрении на животных указывают на наличие окислительно-восстановительного дисбаланса и окислительного стресса при этом заболевании. В совокупности эти данные свидетельствуют, что генетические факторы и факторы окружающей среды влияют на проявление разных патологическихмеханизмов при шизофрении (нарушения нейромедиаторных систем, гипофункцию рецепторов N-метил-D-аспарата (NMDAR), нейровоспаление, нарушение сигнальных каскадов белкового фосфорилирования). Они приводят к окислительному стрессу, который усиливает первоначальные патологические изменения, вследствие чего нарушаются процессы синхронизации и межклеточные связи в головном мозге. В качестве лекарственных препаратов, снижающих вредное воздействие окислительного стресса, могут быть использованы соединения с антиоксидантными и противовоспалительными свойствами, соединения для коррекции митохондриальной дисфункции и модуляторы передачи сигналов, опосредованных NMDAR. Эффективность этих соединений может различаться у разных пациентов, поэтому большое значение имеет разработка системы биомаркеров, нацеленных на выявление лиц, с большей вероятностью реагирующих на конкретный препарат.

   Background

   Background: heterogeneity of schizophrenia is reflected in the variety of clinical manifestations and biological disorders, on the basis of which several neurochemical hypotheses are formulated for schizophrenia pathogenesis. Review of the current hypotheses of schizophrenia pathogenesis shows that oxidative stress is not the main cause of the disease development, but affects its course and contributes to the deterioration of the patient’s condition.

   Objective

   Objective: analysis of the relationships between redox imbalance and oxidative stress and the development of pathological processes in schizophrenia within the framework of neurochemical hypotheses of the disease pathogenesis.

   Material and methods

   Material and methods: a search was made for sources in the Medline/PubMed databases, Scopus and RSCI using keyword combinations “oxidative stress”, “oxidation-reduction imbalance”, “schizophrenia”, “hypotheses of schizophrenia pathogenesis”, “antioxidants”, “neurotransmitters”, “glutathione”, “neuroinflammation”.

   Conclusion

   Conclusion: data from numerous studies of the brain of patients with schizophrenia, their blood plasma, serum, and blood cells as well as the study of animal models of schizophrenia indicate the presence of redox imbalance and oxidative stress in this disease. Taken together, these data indicate that genetic and environmental factors that affect the manifestation of various pathological mechanisms in schizophrenia (disturbances in neurotransmitter systems, hypofunction of N-methyl-D-aspartate receptors, neuroinflammation, impaired signaling protein phosphorylation pathways) lead to the oxidative stress, enhancing the initial pathological changes, as a result of which synchronization processes and intercellular communications in the brain become disrupted. Medicines with antioxidant and anti-inflammatory properties, compounds for correcting mitochondrial dysfunction, and NMDAR-mediated signaling modulators can be used as drugs to reduce the harmful effects of oxidative stress. The efficacy of these medicines may vary in different patients, so the development of biomarker systems aimed at identifying individuals who are more likely to respond to a particular drug is of great importance.

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The authors declare that there are no conflicts of interest present.