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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">glaucoma</journal-id><journal-title-group><journal-title xml:lang="ru">Национальный журнал Глаукома</journal-title><trans-title-group xml:lang="en"><trans-title>National Journal glaucoma</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2078-4104</issn><issn pub-type="epub">2311-6862</issn><publisher><publisher-name>Federal State Budgetary Institution of Science “Krasnov Research Institute of Eye Diseases”</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.25700/NJG.2018.03.10</article-id><article-id custom-type="elpub" pub-id-type="custom">glaucoma-224</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>ОБЗОР ЛИТЕРАТУРЫ</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>REVIEW OF LITERATURE</subject></subj-group></article-categories><title-group><article-title>Теоретическое обоснование нейропротекторной терапии при глаукоме как инволюционно зависимой патологии</article-title><trans-title-group xml:lang="en"><trans-title>Theoretical substantiation of neuroprotective therapy in glaucoma as an involution-dependent pathology</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>Еричев</surname><given-names>В. П.</given-names></name><name name-style="western" xml:lang="en"><surname>Erichev</surname><given-names>V. P.</given-names></name></name-alternatives><bio xml:lang="ru"><p>д.м.н., профессор, руководитель отдела глаукомы.</p><p>119021, Российская Федерация, Москва, ул. Россолимо, 11А. </p></bio><bio xml:lang="en"><p>Med.Sc.D., Professor, Head of Glaucoma Department.</p><p>11A Rossolimo st., Moscow, Russian Federation, 119021. </p></bio><email xlink:type="simple">erichev@reic.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>Панюшкина</surname><given-names>Л. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Panyushkina</surname><given-names>L. A.</given-names></name></name-alternatives><bio xml:lang="ru"><p>к.м.н., младший научный сотрудник отдела глаукомы.</p><p>119021, Российская Федерация, Москва, ул. Россолимо, 11А.</p></bio><bio xml:lang="en"><p>Ph.D., Junior Research Associate of Glaucoma Departmentt.</p><p>11A Rossolimo st., Moscow, Russian Federation, 119021.</p></bio><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru"><institution>ФГБНУ «НИИ глазных болезней».</institution><country>Россия</country></aff><aff xml:lang="en"><institution>Scientific Research Institute of Eye Diseases.</institution><country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2018</year></pub-date><pub-date pub-type="epub"><day>30</day><month>12</month><year>2018</year></pub-date><volume>17</volume><issue>3</issue><fpage>86</fpage><lpage>96</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Еричев В.П., Панюшкина Л.А., 2018</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="ru">Еричев В.П., Панюшкина Л.А.</copyright-holder><copyright-holder xml:lang="en">Erichev V.P., Panyushkina L.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.glaucomajournal.ru/jour/article/view/224">https://www.glaucomajournal.ru/jour/article/view/224</self-uri><abstract><p>Несмотря на эффективную гипотензивную терапию, глаукомная оптическая нейропатия нередко прогрессирует. Возможный патогенетический механизм этой прогрессии — нейродегенерация, объединяющая многие инволюционные заболевания, такие как болезнь Альцгеймера, болезнь Паркинсона и другие. Несмотря на разную этиологию и клиническую картину, всех их объединяет несколько общих признаков, характерных для инволюционных заболеваний: увеличение заболеваемости с возрастом, практически бессимптомное начало и прогрессирующее ухудшение функций, генетическая предрасположенность. Гибель нейронов при всех нейродегенеративных заболеваниях (в том числе и глаукоме) осуществляется по механизму апоптоза, в основе которого лежат следующие патологические процессы: депривация нейротрофических факторов, повышение концентрации возбуждающих аминокислот, окислительный стресс и нейровоспаление. В данном обзоре представлены современные данные об аксональной и транссинаптической нейродегенерации, об оксидативном стрессе и глутаматной эксайтоксичности при глаукоме как ведущих звеньях в распространении патологического процесса и основных мишенях для нейропротекторной терапии.</p></abstract><trans-abstract xml:lang="en"><p>Glaucomatous optic neuropathy in some cases is known to progress despite effective hypotensive therapy. It might be explained by an underlying pathogenic mechanism of neurodegeneration that unites multiple involution-related diseases, such as Alzheimer’s, Parkinson’s and others. Despite differing etiology and clinical picture, they are all united by several common features characteristic of involution-related diseases: age-related morbidity increase, general lack of symptoms at the onset, progressive function deterioration and genetic predisposition. Neuron death in all degenerative diseases including glaucoma follows a common apoptosis mechanism, characterized by the following underlying mechanisms: neurotrophic factor deprivation, excitatory amino acids level increase, oxidative stress and neuroinflammation. This review presents current data on axonal and transsynaptic neurodegeneration, oxidative stress and glutamate exitotoxicity as leading components of the pathological glaucoma process and main targets of neuroprotective therapy.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>глаукома</kwd><kwd>болезнь Альцгеймера</kwd><kwd>болезнь Паркинсона</kwd><kwd>нейродегенерация</kwd><kwd>нейропротекция</kwd><kwd>апоптоз</kwd><kwd>оксидативный стресс</kwd><kwd>эксайтотоксичность</kwd><kwd>диффузионно-тензорная МРТ</kwd><kwd>митохондриальная дисфункция</kwd></kwd-group><kwd-group xml:lang="en"><kwd>glaucoma</kwd><kwd>Alzheimer’s disease</kwd><kwd>Parkinson’s disease</kwd><kwd>neurodegeneration</kwd><kwd>neuroprotection</kwd><kwd>apoptosis</kwd><kwd>oxidative stress</kwd><kwd>exitotoxicity</kwd><kwd>diffusion-tensor MRI</kwd><kwd>mitochondrial dysfunction</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">Quigley H.A., Broman A.T. 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Eye. 2018; 32(5):938-945. doi: 10.1038/s41433-018-0050-2.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
