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<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="review-article" dtd-version="1.2" xml:lang="en"><front><journal-meta><journal-id journal-id-type="publisher-id">Acta Naturae</journal-id><journal-title-group><journal-title xml:lang="en">Acta Naturae</journal-title><trans-title-group xml:lang="ru"><trans-title>Acta Naturae</trans-title></trans-title-group></journal-title-group><issn publication-format="print">2075-8251</issn><publisher><publisher-name xml:lang="en">Acta Naturae Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">10761</article-id><article-id pub-id-type="doi">10.32607/20758251-2010-2-1-72-80</article-id><article-categories><subj-group subj-group-type="toc-heading" xml:lang="en"><subject>Articles</subject></subj-group><subj-group subj-group-type="toc-heading" xml:lang="ru"><subject>Статьи</subject></subj-group><subj-group subj-group-type="article-type"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title xml:lang="en">Calcium Signaling and Neurodegeneration</article-title><trans-title-group xml:lang="ru"><trans-title>Calcium Signaling and Neurodegeneration</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author"><name><surname>Bezprozvanny</surname><given-names>I B</given-names></name><email>Ilya.Bezprozvanny@UTSouthwestern.edu</email><xref ref-type="aff" rid="aff1"/><xref ref-type="aff" rid="aff2"/></contrib></contrib-group><aff-alternatives id="aff1"><aff><institution xml:lang="en">University of Texas Southwestern Medical Center</institution></aff><aff><institution xml:lang="ru"></institution></aff></aff-alternatives><aff id="aff2"><institution>Institute of Cytology, Russian Academy of Sciences</institution></aff><pub-date date-type="pub" iso-8601-date="2010-03-15" publication-format="electronic"><day>15</day><month>03</month><year>2010</year></pub-date><volume>2</volume><issue>1</issue><issue-title xml:lang="en">VOL 2, NO1 (2010)</issue-title><issue-title xml:lang="ru">ТОМ 2, №1 (2010)</issue-title><fpage>72</fpage><lpage>80</lpage><history><date date-type="received" iso-8601-date="2020-01-17"><day>17</day><month>01</month><year>2020</year></date></history><permissions><copyright-statement xml:lang="en">Copyright ©; 2010, Bezprozvanny I.B.</copyright-statement><copyright-statement xml:lang="ru">Copyright ©; 2010, Bezprozvanny I.B.</copyright-statement><copyright-year>2010</copyright-year><copyright-holder xml:lang="en">Bezprozvanny I.B.</copyright-holder><copyright-holder xml:lang="ru">Bezprozvanny I.B.</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://actanaturae.ru/2075-8251/article/view/10761">https://actanaturae.ru/2075-8251/article/view/10761</self-uri><abstract xml:lang="en"><p/></abstract><trans-abstract xml:lang="ru"><p>Neurodegenerative disorders, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and spinocerebellar ataxias (SCA) are very important both for fundamental science and for practical medicine. Despite extensive research into the causes of these diseases, clinical researchers have had very limited progress and, as of now, there is still no cure for any of these diseases. One of the main obstacles in the way of creating treatments for these disorders is the fact that their etiology and pathophysiology still remain unclear. This paper reviews results that support the so-called “calcium hypothesis of neurodegenerative diseases.” The calcium hypothesis states that the atrophic and degenerative processes in the neurons of AD, PD, ALS, HD, and SCA patients are accompanied by alterations in calcium homeostasis. Moreover, the calcium hypothesis states that this deregulation of calcium signaling is one of the early-stage and key processes in the pathogenesis of these diseases. Based on the results we reviewed, we conclude that the calcium channels and other proteins involved in the neuronal calcium signaling system are potential drug targets for AD, PD, ALS, HD, and SCA therapy.</p></trans-abstract><kwd-group xml:lang="en"><kwd>Alzheimer’s disease</kwd><kwd>Parkinson’s disease (PD)</kwd><kwd>amyotrophic lateral sclerosis</kwd><kwd>Huntington’s disease</kwd><kwd>spinocerbellar ataxias</kwd><kwd>calcium channels</kwd><kwd>calcium signaling</kwd><kwd>mitochondria</kwd><kwd>transgenic mice</kwd><kwd>clinical trials</kwd><kwd>imaging</kwd><kwd>memantine</kwd><kwd>dimebon</kwd><kwd>riluzole</kwd></kwd-group></article-meta></front><body></body><back><ref-list><ref id="B1"><label>1.</label><mixed-citation>Berridge M.J. // Neuronal Calcium Signaling. 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