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<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medbio</journal-id><journal-title-group><journal-title xml:lang="ru">Медико-биологические проблемы жизнедеятельности</journal-title><trans-title-group xml:lang="en"><trans-title>Medical and Biological Problems of Life Activity</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2074-2088</issn><publisher><publisher-name>Республиканский научно-практический центр радиационной медицины и экологии человека</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.58708/2074-2088.2024-2(32)-15-22</article-id><article-id custom-type="elpub" pub-id-type="custom">medbio-396</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>ОБЗОРЫ И ПРОБЛЕМНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS AND PROBLEM ARTICLES</subject></subj-group></article-categories><title-group><article-title>Воспаление как движущая сила нейродегенерации. Основы персонифицированной диагностики и лечения (обзор литературы)</article-title><trans-title-group xml:lang="en"><trans-title>Inflammation as a driving force of neurodegeneration. Fundamentals of personalized diagnostics and treatment</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Вист</surname><given-names>Э. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Vist</surname><given-names>E. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ассистент кафедры неврологии и нейрохирургии</p><p>г. Минск</p></bio><email xlink:type="simple">edgar.vist@mail.ru</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Бойко</surname><given-names>А. В.</given-names></name><name name-style="western" xml:lang="en"><surname>Boika</surname><given-names>A. V.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кандидат медицинских наук, доцент кафедры неврологии и нейрохирургии</p><p>г. Минск</p></bio><email xlink:type="simple">AVBoika@yandex.by</email><xref ref-type="aff" rid="aff-1"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Селицкий</surname><given-names>М. М.</given-names></name><name name-style="western" xml:lang="en"><surname>Sialitski</surname><given-names>M. M.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Кандидат медицинских наук, доцент кафедры неврологии и нейрохирургии</p><p>г. Минск</p></bio><email xlink:type="simple">m_sialitski@tut.by</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff xml:lang="ru" id="aff-1"><institution>ИПКП кадров здравоохранения УО «Белорусский государственный медицинский университет»</institution><country>Belarus</country></aff><pub-date pub-type="collection"><year>2024</year></pub-date><pub-date pub-type="epub"><day>20</day><month>09</month><year>2024</year></pub-date><volume>0</volume><issue>2</issue><fpage>15</fpage><lpage>22</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Вист Э.В., Бойко А.В., Селицкий М.М., 2024</copyright-statement><copyright-year>2024</copyright-year><copyright-holder xml:lang="ru">Вист Э.В., Бойко А.В., Селицкий М.М.</copyright-holder><copyright-holder xml:lang="en">Vist E.V., Boika A.V., Sialitski M.M.</copyright-holder><license xml:lang="ru" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>Данная работа распространяется под лицензией Creative Commons Attribution 4.0.</license-p></license><license xml:lang="en" license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://medbio.ejournal.by/jour/article/view/396">https://medbio.ejournal.by/jour/article/view/396</self-uri><abstract><p>ЦНС интегрирует эфферентные сигналы соматической и вегетативной частей. При этом ЦНС получает информацию с периферии о воспалении и инфекции. Цитокины, хемокины и ассоциированные с повреждением растворимые медиаторы системного воспаления могут попасть в ЦНС через кровеносную и/или лимфатическую системы, проникнуть непосредственно через околожелудочковые структуры, посредством повышения проницаемости гематоэнцефалического барьера и нарушить здоровое функционирование нейронов и глии, приводя к нарушению гомеостаза мозга. Это может привести к дебюту нейродегенеративного заболевания или ухудшить его клинические симптомы. В данной публикации мы приводим современные международные научные данные, свидетельствующие о связи между нейродегенеративным процессом и иммунными нарушениями. Кроме указания на иммуноопосредованные пути нейродегенерации, приводятся новые потенциально значимые иммуномодулирующие мишени для разработки возможной эффективной терапии данной группы заболеваний.</p></abstract><trans-abstract xml:lang="en"><p>The CNS integrates efferent signals from the somatic and autonomic parts. Also the CNS also receives information from the periphery about inflammation and infection. Cytokines, chemokines and damage-associated soluble mediators of systemic inflammation can also enter the CNS via the blood and/or lymphatic systems. At the same time these substances can penetrate directly through periventricular structures, as well as by increasing the permeability of the blood-brain barrier and disrupt the healthy functioning of neurons and glia, leading to a violation of brain homeostasis. This can lead to the onset of a neurodegenerative disease or worsen its clinical symptoms. In this publication, we present current international scientific data indicating a link between the neurodegenerative process and immune disorders. In addition to identifying immune-mediated pathways of neurodegeneration, new, potentially significant, immunomodulatory targets are presented for the development of possible effective therapy for this group of diseases.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>воспаление</kwd><kwd>нейродегенеративный процесс</kwd><kwd>патогенез</kwd><kwd>апоптоз</kwd><kwd>болезнь Альцгеймера</kwd></kwd-group><kwd-group xml:lang="en"><kwd>inflammation</kwd><kwd>neurodegeneration</kwd><kwd>pathogenesis</kwd><kwd>apoptosis</kwd><kwd>Alzheimer's disease</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Microglia are polarized to M1 type in highanxiety inbred mice in response to lipopolysaccharide challenge / Z. 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