<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE root>
<article 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" xmlns:ali="http://www.niso.org/schemas/ali/1.0/" article-type="other" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Annals of Clinical and Experimental Neurology</journal-id><journal-title-group><journal-title xml:lang="en">Annals of Clinical and Experimental Neurology</journal-title><trans-title-group xml:lang="ru"><trans-title>Анналы клинической и экспериментальной неврологии</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-5473</issn><issn publication-format="electronic">2409-2533</issn><publisher><publisher-name xml:lang="en">Eco-Vector</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">562</article-id><article-id pub-id-type="doi">10.25692/ACEN.2018.5.7</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Reviews</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Обзоры</subject></subj-group><subj-group subj-group-type="article-type"><subject>Unknown</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Methods of immunohistochemistry and computerized morphometry as promising tools in the study of pathogenic patterns of neurodegenerative processes</article-title><trans-title-group xml:lang="ru"><trans-title>Методы иммуногистохимии и компьютерной морфометрии – перспективные инструменты в изучении патогенетических закономерностей нейродегенеративных процессов</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Khudoerkov</surname><given-names>Rudolf M.</given-names></name><name xml:lang="ru"><surname>Худоерков</surname><given-names>Рудольф Михайлович</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>rolfbrain@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Salkov</surname><given-names>Vladimir N.</given-names></name><name xml:lang="ru"><surname>Сальков</surname><given-names>Владимир Николаевич</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>rolfbrain@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib><contrib contrib-type="author"><name-alternatives><name xml:lang="en"><surname>Voronkov</surname><given-names>Dmitry N.</given-names></name><name xml:lang="ru"><surname>Воронков</surname><given-names>Дмитрий Николаевич</given-names></name></name-alternatives><address><country country="RU">Russian Federation</country></address><email>rolfbrain@yandex.ru</email><xref ref-type="aff" rid="aff1"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">Research Center of Neurology</institution></aff><aff><institution xml:lang="ru">ФГБНУ «Научный центр неврологии»</institution></aff></aff-alternatives><pub-date date-type="pub" iso-8601-date="2018-12-26" publication-format="electronic"><day>26</day><month>12</month><year>2018</year></pub-date><volume>12</volume><issue>5S</issue><issue-title xml:lang="en"/><issue-title xml:lang="ru"/><fpage>55</fpage><lpage>59</lpage><history><date date-type="received" iso-8601-date="2018-12-26"><day>26</day><month>12</month><year>2018</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2018, Khudoerkov R.M., Salkov V.N., Voronkov D.N.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2018, Khudoerkov R.M., Salkov V.N., Voronkov D.N.</copyright-statement><copyright-year>2018</copyright-year><copyright-holder xml:lang="en">Khudoerkov R.M., Salkov V.N., Voronkov D.N.</copyright-holder><copyright-holder xml:lang="ru">Khudoerkov R.M., Salkov V.N., Voronkov D.N.</copyright-holder><ali:free_to_read xmlns:ali="http://www.niso.org/schemas/ali/1.0/"/><license><ali:license_ref xmlns:ali="http://www.niso.org/schemas/ali/1.0/">https://creativecommons.org/licenses/by/4.0</ali:license_ref></license></permissions><self-uri xlink:href="https://annaly-nevrologii.com/pathID/article/view/562">https://annaly-nevrologii.com/pathID/article/view/562</self-uri><abstract xml:lang="en"><p>Modern methods of immunohistochemistry and computer morphometry provide powerful possibilities for the study of pathogenetic patterns of neurodegeneration process occurring in physiological aging of men and women, as well as in experimental animals on modeling of Parkinson’s and Huntington's diseases. Threedimensional reconstruction of the substantia nigra pars compacta of the human and rat brains revealed both common features in their organization (heterogeneity of structures) and differences in quantitative morphochemical parameters determining their species-specific characteristics. On modeling of the Huntington's disease with the neurotoxin 3-nitropropionic acid (3-NPA), it was shown not only the death of neurons in the striatum and a decrease in its dopaminergic innervation, but also dysfunction of astrocytes with reduced expression of glutamine synthase that can increase the extracellular content of glutamate. The latter,along with direct succinate dehydrogenase-blocking action of 3-NPA, is one of the factors leading to neurodegenerative changes in the striatum. On modeling of Parkinson's disease, the important role of neuroglia in the neurodegenerative process was shown: it was found that activated astroglia had not only destructive, but also neuroprotective functions, which may serve the basis for the development of respective methods of pharmacological correction directed at regulation of the of glial cell functions.</p></abstract><trans-abstract xml:lang="ru"><p>Современные методы иммуногистохимии и компьютерной морфометрии дают богатые возможности для изучения патогенетических закономерностей процесса нейродегенерации, происходящего при физиологическом старении мужчин и женщин, а также при моделировании болезней Паркинсона и Гентингтона у экспериментальных животных. Трехмерная реконструкция компактной части черной субстанции мозга человека и мозга крысы выявила как общие черты в их организации (гетерогенность структур), так и различия в количественных морфохимических показателях, обусловливающих их видоспецифические характеристики. При моделировании болезни Гентингтона с помощью нейротоксина 3-нитропропионовой кислоты (3-НПК) была показана не только гибель нейронов стриатума и снижение его дофаминергической иннервации, но и повреждение астроцитов со снижением в них экспрессии глутаминсинтетазы, что может увеличивать содержание внеклеточного глутамата. Последний, наряду с прямым блокирующим действием 3-НПК на сукцинатдегидрогеназу, является одним из факторов формирования нейродегенеративных изменений в стриатуме. При моделировании болезни Паркинсона была показана важная роль нейроглии в нейродегенеративном процессе: выявлено, что активированная астроглия выполняет не только деструктивную, но и нейропротекторную функцию, что может служить основой для разработки соответствующих методов фармакологической коррекции, направленных на регуляцию функций глиальных клеток.</p></trans-abstract><kwd-group xml:lang="en"><kwd>human brain</kwd><kwd>rat brain</kwd><kwd>substantia nigra</kwd><kwd>neuron</kwd><kwd>neuroglia</kwd><kwd>immunohistochemistry</kwd><kwd>morphometry</kwd><kwd>3D reconstruction</kwd></kwd-group><kwd-group xml:lang="ru"><kwd>мозг человека</kwd><kwd>мозг крысы</kwd><kwd>черная субстанция</kwd><kwd>нейроны</kwd><kwd>нейроглия</kwd><kwd>иммуногистохимия</kwd><kwd>морфометрия</kwd><kwd>3D реконструкция</kwd></kwd-group><funding-group/></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><citation-alternatives><mixed-citation xml:lang="en">Illarioshkin S.N. [Current view on etiology of Parkinson’’s disease]. Nevrologicheskiy zhurnal 2015; 4: 4–13. (In Russ.).</mixed-citation><mixed-citation xml:lang="ru">Иллариошкин С.Н. Современные представления об этиологии болезни Паркинсона. Неврологический журнал 2015; 4: 4–13.</mixed-citation></citation-alternatives></ref><ref id="B2"><label>2.</label><mixed-citation>Khudoerkov R.M., Voronkov D.N. Quantitative assessment of neurons and neuroglia with computer morphometry. Bull Exp Biol Med 2010; 149: 100–103. PMID: 21113470.</mixed-citation></ref><ref id="B3"><label>3.</label><mixed-citation>Blesa J., Przedborski S. Parkinson’s disease: animal models and dopaminergic cell vulnerability. Front Neuroanat 2014; 8: 1–12. DOI: 10.3389/ fnana.2014.00155. PMID: 25565980.</mixed-citation></ref><ref id="B4"><label>4.</label><mixed-citation>Brichta L., Greengard P. Molecular determinants of selective dopaminergic vulnerability in Parkinson’s disease: an update. Front Neuroanat 2014; 8: 152. DOI: 10.3389/fnana.2014.00152. PMID: 25565977.</mixed-citation></ref><ref id="B5"><label>5.</label><mixed-citation>Damier P., Hirsch E.С., Agid Y., Graybiel A.M. The substantia nigra of the human brain. I. Nigrosomes and nigral matrix, a compartmental organization based on calbindin D28k immunogistochemistry. Brain 1999; 122: 1421–1436. DOI: 1093/brain/122.8.1421. PMID:10430829.</mixed-citation></ref><ref id="B6"><label>6.</label><mixed-citation>Bellinger F.P., Bellinger M.T., Seale L.A. et al. Glutathione peroxidase 4 is associated with neuromelanin in substantia nigra and dystrophic axons in putamen of Parkinson’s brain. Mol Neurodeg 2011; 6: 1–8. DOI: 10.1186/1750-1326-6-8. PMID: 21255396.</mixed-citation></ref><ref id="B7"><label>7.</label><mixed-citation>Brouillet, E., Jacquard, C., Bizat, N., Blum, D., 3-Nitropropionic acid: a mitochondrial toxin to uncover physiopathological mechanisms underlying striatal degeneration in Huntington’s disease. J Neurochem 2005; 95(6): 1521.</mixed-citation></ref><ref id="B8"><label>8.</label><mixed-citation>Jellinger K.A. Neuropathobiology of non-motor symptoms in Parkinson disease. J Neural Transm 2015; 122: 1429–1440. DOI: 10.1007/s00702-015-1405-5. PMID: 25976432.</mixed-citation></ref><ref id="B9"><label>9.</label><mixed-citation>Jyothi H.J., Vidyadhara D.J., Mahadevan A. et al. Aging causes morphological alterations in astrocytes and microglia in human substantia nigra pars compacta. Neurobiol Aging 2015; 36: 3321–3333. DOI: 0.1016/j.neurobiolaging. 2015.08.024. PMID: 26433682.</mixed-citation></ref><ref id="B10"><label>10.</label><mixed-citation>Kordower J.H., Olanow C.W., Dodiya H.B. et al. Disease duration and the integrity of the nigrostriatal system in Parkinson’s disease. Brain 2013; 136: 2419–2431. DOI: 10.1093/brain/awt192. PMID: 23884810.</mixed-citation></ref><ref id="B11"><label>11.</label><mixed-citation>Rudow G., O’Brien R., Savonenko A.V.et al. Morphometry of the human substantia nigra in ageing and Parkinson’s disease. Acta Neuropathol 2008; 115: 461–470. DOI: 10.1007/s00401-008-0352-8. PMID: 18297291.</mixed-citation></ref><ref id="B12"><label>12.</label><mixed-citation>Zucca F.A., Giaveri G., Gallorini M. et al. The neuromelanin of human substantia nigra: physiological and pathogenic aspects. Pigment Cell Res 2004; 17: 610–617. DOI: 10.1111/j.1600-0749.2004.00201.x. PMID: 15541018.</mixed-citation></ref></ref-list></back></article>
