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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">r-n-j</journal-id><journal-title-group><journal-title xml:lang="ru">Российский неврологический журнал</journal-title><trans-title-group xml:lang="en"><trans-title>Russian neurological journal</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2658-7947</issn><issn pub-type="epub">2686-7192</issn><publisher><publisher-name>МИА</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.30629/2658-7947-2025-30-6-11-20</article-id><article-id custom-type="elpub" pub-id-type="custom">r-n-j-772</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</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Роль старения в терапии болезни Альцгеймера</article-title><trans-title-group xml:lang="en"><trans-title>Role of Ageing in Alzheimer's Therapeutics</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid">https://orcid.org/0000-0001-9357-4983</contrib-id><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Абдель-Сатер</surname><given-names>Х. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Abdel-Sater</surname><given-names>Kh. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>cтоматологический факультет; кафедра медицинских и стоматологических наук</p><p>Эль-Карак</p></bio><bio xml:lang="en"><p>Faculty of Dentistry; Department of Dental and Medical Sciences</p><p>Al-Karak</p></bio><email xlink:type="simple">Kabdelsater@mutah.edu.jo</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>Университет Мута</institution><country>Иордания</country></aff><aff xml:lang="en"><institution>Mutah University</institution><country>Jordan</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2025</year></pub-date><pub-date pub-type="epub"><day>12</day><month>02</month><year>2026</year></pub-date><volume>30</volume><issue>6</issue><fpage>11</fpage><lpage>20</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Абдель-Сатер Х.А., 2026</copyright-statement><copyright-year>2026</copyright-year><copyright-holder xml:lang="ru">Абдель-Сатер Х.А.</copyright-holder><copyright-holder xml:lang="en">Abdel-Sater K.A.</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://www.r-n-j.com/jour/article/view/772">https://www.r-n-j.com/jour/article/view/772</self-uri><abstract><sec><title>   Введение</title><p>   Введение. Наиболее значимым фактором риска болезни Альцгеймера (БА) является старение, которое способствует нарушению клиренса тау-протеина и амилоида-β (Aβ) белков, сенесценции микроглии, стрессу эндоплазматического ретикулума (ЭР), дисрегуляции липидов и иксайтотоксичности. В обзоре рассматривается, как старение ускоряет патофизиологические механизмы БА, а также оцениваются новые научные (geroscience) подходы, направленные на изучение биологических процессов старения с целью задержки или предотвращения когнитивного снижения.</p></sec><sec><title>   Материал и методы</title><p>   Материал и методы. Проведен нарративный обзор литературы за период 2015–2025 гг. с интеграцией данных лонгитюдных исследований, метаанализов и доклинических моделей, изучающих взаимосвязь старения и БА. Поисковые запросы в базах MED-LINE, Embase, Cochrane, Google Scholar и PubMed включали ключевые слова: старение, БА, патология БА, антиэйджинг-стратегии и терапия БА.</p></sec><sec><title>   Результаты</title><p>   Результаты. На этапе первичного поиска было исключено более 150 исследований, и только 100 работ были отобраны для дальнейшего анализа. После дополнительной проверки были удалены 30 дублирующих исследований. В конечном итоге обзор включил 70 исследований. Большинство из них рассматривали механизмы, связанные со старением — дисфункцию глимфатической системы, нарушение транспорта липидов, связанное с APOE ε4, снижение уровня BDNF и глутамат-опосредованную иксайтотоксичность, а также антиэйджинг-стратегии, включая изменения образа жизни (физическая активность, оптимизация сна, когнитивная активность) и медицинские или биологические терапии БА.</p></sec><sec><title>   Заключение</title><p>   Заключение. Нацеливание на механизмы старения представляет собой смену парадигмы в профилактике и лечении БА; однако для внедрения геронауки в клиническую практику необходима междисциплинарная работа. Интеграция стратегий образа жизни и фармакологических вмешательств может обеспечить синергетическую нейропротекцию. Будущие исследования должны быть сосредоточены на интегрированных мультимодальных подходах, сочетающих модификацию образа жизни, и биологическими методами лечения. Индивидуализированные стратегии – основанные на генетическом риске (например, статус APOE), сопутствующих заболеваниях и индивидуальных траекториях старения – могут оптимизировать результаты. Для оценки долгосрочной безопасности и эффективности инновационных вмешательств, таких как сенолитики, эпигенетические модуляторы и стволовые клеточные терапии, необходимы крупные длительные клинические исследования. Прогресс в области биомаркеров биологического возраста, машинного обучения и системной биологии может улучшить оценку риска и персонализацию терапии.</p></sec></abstract><trans-abstract xml:lang="en"><sec><title>   Background</title><p>   Background. The biggest risk factor for Alzheimer’s disease (AD) is aging, contributing to impaired clearance of tau and amyloid-beta (Aβ) proteins, microglial senescence, endoplasmic reticulum (ER) stress, lipid dysregulation, and excitotoxicity. Objective. This review investigates how aging speeds up the pathophysiology of AD and evaluates emerging geroscience-based interventions targeting biological aging mechanisms to delay or prevent cognitive decline.</p></sec><sec><title>   Material and methods</title><p>   Material and methods. A narrative review of the literature from 2015 to 2025 was conducted, integrating longitudinal studies, meta-analyses, and preclinical models that examine the aging — AD interface. The MEDLINE, Embase, Cochrane, Google Scholar, and PubMed databases were searched using specifi cally related keywords, such as ageing, AD, AD pathology, anti-aging strategies, and AD therapies.</p></sec><sec><title>   Results</title><p>   Results. From the initial search, more than 150 studies were excluded, and only 100 studies were selected for this review. After revision also duplicated 30 studies were removed. Ultimately, the review comprised seventy studies. Most of these studies discussed aging-related mechanisms — glymphatic dysfunction, APOE ε4-associated lipid transport impairment, BDNF depletion, and glutamate excitotoxicity, and anti-ageing strategies such as lifestyle interventions (e.g., physical activity, sleep optimization, cognitive engagement) and medical and biological therapies for AD.</p></sec><sec><title>   Conclusion</title><p>   Conclusion. Targeting aging mechanisms offers a paradigm shift in AD prevention and treatment; however, multidisciplinary collaboration is essential to translate geroscience into clinical practice. The integration of lifestyle and pharmacological strategies may yield synergistic neuroprotective benefi ts. Future research should focus on integrated, multimodal interventions that combine lifestyle modification with pharmacological and biological therapies. Tailored approaches — based on genetic risk profi les (e.g., APOE status), comorbidities, and individual aging trajectories — may optimize clinical outcomes. To evaluate the long-term safety and effectiveness of innovative treatments like senolytics, epigenetic modulators, and stem cell-based therapies in older populations, extensive, longitudinal clinical trials are also required. Developments in biological age biomarkers, machine learning, and systems biology have the potential to improve risk assessment and therapy customization.</p></sec></trans-abstract><kwd-group xml:lang="ru"><kwd>болезнь Альцгеймера</kwd><kwd>старение</kwd><kwd>нейровоспаление</kwd><kwd>сенолитики</kwd><kwd>эпигенетика</kwd><kwd>стволовая терапия</kwd></kwd-group><kwd-group xml:lang="en"><kwd>Alzheimer’s disease</kwd><kwd>aging</kwd><kwd>neuroinflammation</kwd><kwd>senolytics</kwd><kwd>epigenetics</kwd><kwd>stem cell therapy</kwd></kwd-group><funding-group><funding-statement xml:lang="ru">Исследование выполнено без финансовой поддержки</funding-statement><funding-statement xml:lang="en">The study had no sponsorship</funding-statement></funding-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Scheltens P, De Strooper B, Kivipelto M, Holstege H, Chételat G, Teunissen CE, Cummings J, van der Flier WM. 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