r-n-jРоссийский неврологический журналRussian neurological journal2658-79472686-7192МИА10.30629/2658-7947-2022-27-3-64-73r-n-j-323Research ArticleЛЕКЦИЯLECTUREИнфекционная гипотеза нейродегенеративных заболеваний. Что может ждать нас после пандемии COVID-19?Infectious hypothesis of neurodegenerative diseases. What waits us after the COVID-19 pandemic?https://orcid.org/0000-0001-8988-3011ЛитвиненкоИ. В.LitvinenkoI. V.

Санкт-Петербург

St. Petersburg

litvinenkoiv@rambler.ruhttps://orcid.org/0000-0003-3109-8795ЛобзинВ. Ю.LobzinV. Yu.

Санкт-Петербург

St. Petersburg

vladimirlobzin@mail.ruhttps://orcid.org/0000-0003-3715-2553ПушкарёвВ. А.PushkarevV. A.

Санкт-Петербург

St. Petersburg

vladimirpush@yandex.ruhttps://orcid.org/0000-0002-7218-9346СкрипченкоН. В.SkripchenkoN. V.

Санкт-Петербург

St. Petersburg

snv@niidi.ruВоенно-медицинская академия имени С.М. КироваРоссияMilitary Medical Academy named after S.M. KirovRussian FederationВоенно-медицинская академия имени С.М. Кирова; Детский научно-клинический центр инфекционных болезнейРоссияMilitary Medical Academy named after S.M. Kirov; Children’s Research and Clinical Center for Infectious DiseasesRussian FederationДетский научно-клинический центр инфекционных болезнейРоссияChildren’s Research and Clinical Center for Infectious DiseasesRussian Federation2022140720222736473Copyright © Литвиненко И.В., Лобзин В.Ю., Пушкарёв В.А., Скрипченко Н.В., 20222022Литвиненко И.В., Лобзин В.Ю., Пушкарёв В.А., Скрипченко Н.В.Litvinenko I.V., Lobzin V.Y., Pushkarev V.A., Skripchenko N.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.r-n-j.com/jour/article/view/323

С момента описания первых клинических случаев наиболее распространенных на сегодняшний день нейродегенеративных заболеваний предложены многочисленные гипотезы их развития. В то же время безуспешность терапевтических стратегий в разнообразных направлениях клинических исследований свидетельствует об ошибочности большинства теорий. В связи с этим в последние годы все чаще рассматриваются различные инфекционные агенты в качестве триггера нейронального воспаления и фактора, индуцирующего начало нейродегенеративного процесса. Инфекционные агенты различаются по механизмам инвазии в центральную нервную систему и могут проникать в головной мозг даже периневрально. Реактивация латентной вирусной инфекции индуцирует продукцию вирусных белков и накопление патологических белков, являющихся маркерами болезни Альцгеймера и болезни Паркинсона. Рассматриваются как бактериальные (хламидии, возбудители хронического периодонтита, кишечная палочка), так и вирусные (вирусы герпетической группы, норовирусы) инфекционные агенты. Однако для развития нейродегенерации недостаточно лишь простой инвазии и реактивации инфекционного процесса: огромную роль играют и генетические особенности главного комплекса гистосовместимости. В настоящее время инициированы несколько исследований возможной эффективности антибактериальных и противовирусных препаратов при болезни Альцгеймера. Данные, полученные за последний год, свидетельствуют о том, что головной мозг может выступать в качестве «мишени» для SARS-CoV-2. Неврологические проявления COVID-19 могут возникать в результате как прямого цитопатического действия возбудителя, так и активации нейровоспаления, сопровождающегося при этом нарушением целостности гематоэнцефалического барьера. Дальнейшее изучение молекулярных и клеточных механизмов нейровоспаления и нейродегенерации при COVID-19 послужит основой для разработки методов лечения неврологических осложнений.

Since the description of the first clinical cases of the most common neurodegenerative diseases, numerous hypotheses have been proposed for their development. At the same time, the failure of therapeutic strategies in various directions of clinical research indicates the fallacy of most theories. In this regard, in recent years, various infectious agents are increasingly considered as a trigger of neuronal inflammation and a factor inducing the onset of the neurodegenerative process. Infectious agents differ in their mechanisms of invasion into the central nervous system and can even enter the brain perineurally. Reactivation of latent viral infection induces the production of viral proteins and the accumulation of abnormal proteins that are markers of Alzheimer’s disease and Parkinson’s disease. Both bacterial (chlamydia, causative agents of chronic periodontitis, E. coli) and viral (herpes viruses, noroviruses) infectious agents are considered. However, for the development of neurodegeneration, it is not enough just a simple invasion and reactivation of the infectious process: the genetic characteristics of the main histocompatibility complex also play a huge role. Currently, several studies have been initiated on the possible efficacy of antibacterial and antiviral drugs in Alzheimer’s disease. Data obtained over the past year suggests that the brain may act as a target for SARS-CoV-2. Neurological manifestations of COVID-19 can occur as a result of both the direct cytopathic action of the pathogen and the activation of neuroinflammation, accompanied by a violation of the integrity of the blood-brain barrier. Further study of the molecular and cellular mechanisms of neuroinflammation and neurodegeneration in COVID-19 will form the basis for the development of treatments for neurological complications.

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