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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">anatomy</journal-id><journal-title-group><journal-title xml:lang="ru">Журнал анатомии и гистопатологии</journal-title><trans-title-group xml:lang="en"><trans-title>Journal of Anatomy and Histopathology</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2225-7357</issn><publisher><publisher-name>N.N. Burdenko Voronezh State Medical University</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.18499/2225-7357-2020-9-1-77-85</article-id><article-id custom-type="elpub" pub-id-type="custom">anatomy-1073</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>ОБЗОРНЫЕ СТАТЬИ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW ARTICLES</subject></subj-group></article-categories><title-group><article-title>Морфофункциональные изменения и компенсаторные механизмы в головном мозге человека при старении и болезни Альцгеймера</article-title><trans-title-group xml:lang="en"><trans-title>Morphofunctional Changes and Compensatory Mechanisms in the Human Brain with Aging and in Alzheimer's Disease</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>Ишунина</surname><given-names>Т. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Ishunina</surname><given-names>T. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Ишунина Татьяна Александровна.</p><p>ул. Карла Маркса, 3, г. Курск, 305041, Российская Федерация.</p></bio><bio xml:lang="en"><p>Tat'yana Ishunina.</p><p>ul. Karla Marksa, 3, Kursk, 305041, Russian Federation.</p></bio><email xlink:type="simple">ishunina@gmail.com</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>Боголепова</surname><given-names>И. Н.</given-names></name><name name-style="western" xml:lang="en"><surname>Bogolepova</surname><given-names>I. N.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Москва.</p></bio><bio xml:lang="en"><p>Moscow.</p></bio><xref ref-type="aff" rid="aff-2"/></contrib><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Свааб</surname><given-names>Д. Ф.</given-names></name><name name-style="western" xml:lang="en"><surname>Swaab</surname><given-names>D. F.</given-names></name></name-alternatives><bio xml:lang="ru"><p>Амстердам.</p></bio><bio xml:lang="en"><p>Amsterdam.</p></bio><xref ref-type="aff" rid="aff-3"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБОУ ВО «Курский государственный медицинский университет» Минздрава России</institution></aff><aff xml:lang="en"><institution>Kursk State Medical University</institution></aff></aff-alternatives><aff-alternatives id="aff-2"><aff xml:lang="ru"><institution>ФГБНУ «Научный центр неврологии»</institution></aff><aff xml:lang="en"><institution>Research Center of Neurology</institution></aff></aff-alternatives><aff-alternatives id="aff-3"><aff xml:lang="ru"><institution>Нидерландский институт нейронаук</institution></aff><aff xml:lang="en"><institution>Netherlands Institute for Neuroscience</institution></aff></aff-alternatives><pub-date pub-type="collection"><year>2020</year></pub-date><pub-date pub-type="epub"><day>01</day><month>04</month><year>2020</year></pub-date><volume>9</volume><issue>1</issue><fpage>77</fpage><lpage>85</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Ишунина Т.А., Боголепова И.Н., Свааб Д.Ф., 2020</copyright-statement><copyright-year>2020</copyright-year><copyright-holder xml:lang="ru">Ишунина Т.А., Боголепова И.Н., Свааб Д.Ф.</copyright-holder><copyright-holder xml:lang="en">Ishunina T.A., Bogolepova I.N., Swaab D.F.</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://anatomy.elpub.ru/jour/article/view/1073">https://anatomy.elpub.ru/jour/article/view/1073</self-uri><abstract><p>Статья посвящена обзору возрастных морфофункциональных изменений в головном мозге человека и вопросу компенсаторно-приспособительных механизмов в процессе нормального старения. Согласно данным научной литературы, при старении в большей степени сокращается объем белого вещества, что связано с дегенерацией миелиновых волокон, появлением пространств Вирхова–Робина и снижением эффективности гематоэнцефалического барьера. Атрофические процессы в сером веществе в настоящее время связывают не только с гибелью нейронов, а с дегенеративными изменениями синапсов, уменьшением их количества, редукцией дендритических ветвлений и шипиков. В некоторых структурах головного мозга отмечают снижение размеров перикарионов, приводящее к сокращению численности крупных нейроцитов и увеличению доли мелких нейронов. Однако, в ядрах гипоталамуса, базальном ядре Мейнерта наблюдается возрастная гипертрофия нейронов, в большей степени представленная в группе женщин, где она, несомненно, связана со снижением уровня эстрогенов и периодом наступления менопаузы. Увеличение метаболической активности нейронов, проявляющееся соответствующими изменениями размеров перикарионов и ядер нейронов и их комплекса Гольджи, можно отнести к компенсаторно- приспособительным механизмам, способным задержать или предотвратить развитие нейродегенеративных заболеваний, таких как болезнь Альцгеймера. Нейроны с более высоким уровнем метаболической активности обладают лучшей способностью к саморепарации. В связи с этим, разрабатываются методики реактивации нейронов при старении, основанные на подборе корректного стимула. Компенсаторным следует считать и рост популяции глиальных клеток, имеющих важнейшее значение для адаптации нейронов и способных влиять на уровень синтеза нейрональной РНК. Помимо рассмотрения компенсаторных возможностей головного мозга, в статье приводятся данные литературы о возможных причинах включения этих механизмов при старении и патологических процессах.</p></abstract><trans-abstract xml:lang="en"><p>The article focuses on age-related morphofunctional changes in the human brain and the issue of compensatory-adaptive mechanisms developed in normal aging. According to the scientific literature, the volume of white matter is reduced to a greater extent with aging, the fact associating with myelin fibers degeneration, the appearance of Virchow–Robin spaces and a decrease in the effectiveness of the blood-brain barrier. Atrophic processes in gray matter are currently associated not only with the death of neurons, but with degenerative changes in synapses, a decrease in their number, and reduction of dendritic branches and spines. A decrease in the size of pericarions resulting in a decrease in the number of large neurocytes and an increase in the proportion of small neurons is noted in certain brain structures. However, age-related neuronal hypertrophy is observed in the nuclei of the hypothalamus, Meinert’s basal nucleus. This is mostly manifested in the female group, and is undoubtedly associated with a decrease in estrogen levels and the period of menopause. An increase in the metabolic activity of neurons manifested by related changes in the size of the pericarions and nuclei of neurons and their Golgi complex can be attributed to compensatory-adaptive mechanisms that can delay or prevent the development of neurodegenerative disorders, such as Alzheimer's disease. Neurons with a higher metabolic activity have better ability to self-repair. Due to this, neuron reactivation techniques are being developed with aging based on the selection of the correct stimulus. The growth of the glial cell population is also considered to be compensatory, since these cells are crucial for neuron adaptation and able to affect the level of neuronal RNA synthesis. Furthermore, the article highlights literature data on possible triggers of the compensatory capabilities of the brain with aging and under pathological processes.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>головной мозг</kwd><kwd>старение</kwd><kwd>серое вещество</kwd><kwd>белое вещество</kwd><kwd>болезнь Альцгеймера</kwd><kwd>нейроны</kwd></kwd-group><kwd-group xml:lang="en"><kwd>brain</kwd><kwd>aging</kwd><kwd>white matter</kwd><kwd>gray matter</kwd><kwd>Alzheimer disease</kwd><kwd>neurons</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">Агапов П.А., Боголепова И.Н., Малофеева Л.И. Изменение толщины коры поля 7 верхней теменной области мозга мужчин и женщин в процессе старения. 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