Review: Cell cycle aberrations and neurodegeneration
Identifieur interne : 002862 ( Main/Corpus ); précédent : 002861; suivant : 002863Review: Cell cycle aberrations and neurodegeneration
Auteurs : D. J. Bonda ; V. P. Baji ; B. Spremo-Potparevic ; G. Casadesus ; X. Zhu ; M. A. Smith ; H. LeeSource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 2010-04.
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Abstract
D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.
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DOI: 10.1111/j.1365-2990.2010.01064.x
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J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>D. J. Bonda</name><affiliations><json:string>Departments of Pathology and</json:string></affiliations></json:item><json:item><name>V. P. Bajić</name><affiliations><json:string>Institute of Biomedical Research, Galenika a.d., and</json:string></affiliations></json:item><json:item><name>B. Spremo‐Potparevic</name><affiliations><json:string>Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia</json:string></affiliations></json:item><json:item><name>G. Casadesus</name><affiliations><json:string>Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA;</json:string></affiliations></json:item><json:item><name>X. Zhu</name><affiliations><json:string>Departments of Pathology and</json:string></affiliations></json:item><json:item><name>M. A. Smith</name><affiliations><json:string>Departments of Pathology and</json:string></affiliations></json:item><json:item><name>H.‐G. Lee</name><affiliations><json:string>Departments of Pathology and</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cell cycle re‐entry</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mitotic insult</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mitotic steady state</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oxidative stress</value></json:item></subject><articleId><json:string>NAN1064</json:string></articleId><language><json:string>eng</json:string></language><abstract>D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. 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J.</forename><surname>Bonda</surname></persName><affiliation>Departments of Pathology and</affiliation></author><author><persName><forename type="first">V. P.</forename><surname>Bajić</surname></persName><affiliation>Institute of Biomedical Research, Galenika a.d., and</affiliation></author><author><persName><forename type="first">B.</forename><surname>Spremo‐Potparevic</surname></persName><affiliation>Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia</affiliation></author><author><persName><forename type="first">G.</forename><surname>Casadesus</surname></persName><affiliation>Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA;</affiliation></author><author><persName><forename type="first">X.</forename><surname>Zhu</surname></persName><affiliation>Departments of Pathology and</affiliation></author><author><persName><forename type="first">M. A.</forename><surname>Smith</surname></persName><note type="correspondence"><p>Correspondence: Mark A. Smith, Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 3670; Fax: +1 216 368 8964; E‐mail:</p></note><affiliation>Departments of Pathology and</affiliation></author><author><persName><forename type="first">H.‐G.</forename><surname>Lee</surname></persName><affiliation>Departments of Pathology and</affiliation></author></analytic><monogr><title level="j">Neuropathology and Applied Neurobiology</title><idno type="pISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><idno type="DOI">10.1111/(ISSN)1365-2990</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-04"></date><biblScope unit="volume">36</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="157">157</biblScope><biblScope unit="page" to="163">163</biblScope></imprint></monogr><idno type="istex">0D92870C1B42E891024D4B0C22C10B08D163E8F2</idno><idno type="DOI">10.1111/j.1365-2990.2010.01064.x</idno><idno type="ArticleID">NAN1064</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Alzheimer disease</term></item><item><term>cell cycle re‐entry</term></item><item><term>mitotic insult</term></item><item><term>mitotic steady state</term></item><item><term>oxidative stress</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/0D92870C1B42E891024D4B0C22C10B08D163E8F2/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2990</doi><issn type="print">0305-1846</issn><issn type="electronic">1365-2990</issn><idGroup><id type="product" value="NAN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY APPLIED NEUROBIOLOGY">Neuropathology and Applied Neurobiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="04002"><doi origin="wiley">10.1111/nan.2010.36.issue-2</doi><numberingGroup><numbering type="journalVolume" number="36">36</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2010-04">April 2010</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="6" status="forIssue"><doi origin="wiley">10.1111/j.1365-2990.2010.01064.x</doi><idGroup><id type="unit" value="NAN1064"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Review articles</title></titleGroup><copyright>© 2010 Blackwell Publishing Ltd</copyright><eventGroup><event type="firstOnline" date="2010-01-06"></event><event type="publishedOnlineFinalForm" date="2010-03-23"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText source:FullText result:FullText" date="2010-07-19"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="157">157</numbering><numbering type="pageLast" number="163">163</numbering></numberingGroup><correspondenceTo>Mark A. Smith, Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 3670; Fax: +1 216 368 8964; E‐mail: <email>mark.smith@case.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NAN.NAN1064.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 30 September 2009Accepted after revision 22 December 2009Published online Article Accepted on 6 January 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="60"></count><count type="wordTotal" number="4683"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Review: Cell cycle aberrations and neurodegeneration</title><title type="shortAuthors">D. J. 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A.</givenNames><familyName>Smith</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>H.‐G.</givenNames><familyName>Lee</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Departments of Pathology and</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA;</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Institute of Biomedical Research, Galenika a.d., and</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="RS"><unparsedAffiliation>Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Alzheimer disease</keyword><keyword xml:id="k2">cell cycle re‐entry</keyword><keyword xml:id="k3">mitotic insult</keyword><keyword xml:id="k4">mitotic steady state</keyword><keyword xml:id="k5">oxidative stress</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) <i>Neuropathology and Applied Neurobiology</i><b>36,</b> 157–163
<b>Cell cycle aberrations and neurodegeneration</b></p><p>The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Review: Cell cycle aberrations and neurodegeneration</title></titleInfo><titleInfo type="abbreviated"><title>Cell cycle and neurodegeneration</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Review: Cell cycle aberrations and neurodegeneration</title></titleInfo><name type="personal"><namePart type="given">D. J.</namePart><namePart type="family">Bonda</namePart><affiliation>Departments of Pathology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V. P.</namePart><namePart type="family">Bajić</namePart><affiliation>Institute of Biomedical Research, Galenika a.d., and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Spremo‐Potparevic</namePart><affiliation>Department of Physiology, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Casadesus</namePart><affiliation>Neurosciences, Case Western Reserve University, Cleveland, Ohio, USA;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">X.</namePart><namePart type="family">Zhu</namePart><affiliation>Departments of Pathology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. A.</namePart><namePart type="family">Smith</namePart><affiliation>Departments of Pathology and</affiliation><description>Correspondence: Mark A. Smith, Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. Tel: +1 216 368 3670; Fax: +1 216 368 8964; E‐mail: </description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.‐G.</namePart><namePart type="family">Lee</namePart><affiliation>Departments of Pathology and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-04</dateIssued><edition>Received 30 September 2009Accepted after revision 22 December 2009Published online Article Accepted on 6 January 2010</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="references">60</extent><extent unit="words">4683</extent></physicalDescription><abstract lang="en">D. J. Bonda, V. P. Bajić, B. Spremo‐Potparevic, G. Casadesus, X. Zhu, M. A. Smith and H.‐G. Lee (2010) Neuropathology and Applied Neurobiology36, 157–163
Cell cycle aberrations and neurodegeneration The cell cycle is a highly regulated and fundamental cellular process that involves complex feedback regulation of many proteins, and any compromise to its integrity elicits dire consequences for the cell. For example, in neurodegenerative diseases such as Alzheimer disease (AD), evidence for abnormal cell cycle re‐entry precedes other hallmarks of disease and as such, implicates cell cycle aberrations in the aetiology of AD. The mechanism(s) for cell cycle re‐entry in AD, however, remain unclear. Current theory suggests it to be part of a combination of early events that together elicit the degenerative pathology and cognitive phenotype consistent with the disease. We propose a ‘Two‐Hit Hypothesis’ that highlights the concerted interaction between cell cycle alterations and oxidative stress that combine to produce neurodegeneration. Here, we review the evidence implicating cell cycle mechanisms in AD and how such changes, especially in combination with oxidative stress, would lead to a cascade of events leading to disease. Based on this concept, we propose new opportunities for disease treatment.</abstract><subject lang="en"><genre>Keywords</genre><topic>Alzheimer disease</topic><topic>cell cycle re‐entry</topic><topic>mitotic insult</topic><topic>mitotic steady state</topic><topic>oxidative stress</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology and Applied Neurobiology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0305-1846</identifier><identifier type="eISSN">1365-2990</identifier><identifier type="DOI">10.1111/(ISSN)1365-2990</identifier><identifier type="PublisherID">NAN</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>36</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>157</start><end>163</end><total>7</total></extent></part></relatedItem><identifier type="istex">0D92870C1B42E891024D4B0C22C10B08D163E8F2</identifier><identifier type="DOI">10.1111/j.1365-2990.2010.01064.x</identifier><identifier type="ArticleID">NAN1064</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 Blackwell Publishing Ltd</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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