Oxidative Stress in Parkinson's Disease
Identifieur interne : 000A16 ( Main/Corpus ); précédent : 000A15; suivant : 000A17Oxidative Stress in Parkinson's Disease
Auteurs : Chun Zhou ; Yong Huang ; Serge PrzedborskiSource :
- Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders [ 0077-8923 ] ; 2008-12.
English descriptors
Abstract
Parkinson's disease (PD) is a common adult‐onset neurodegenerative disorder. Typically PD is a sporadic neurological disorder, and over time affected patients see their disability growing and their quality of life declining. Oxidative stress has been hypothesized to be linked to both the initiation and the progression of PD. Preclinical findings from both in vitro and in vivo experimental models of PD suggest that the neurodegenerative process starts with otherwise healthy neurons being hit by some etiological factors, which sets into motion a cascade of deleterious events. In these models initial molecular alterations in degenerating dopaminergic neurons include increased formation of reactive oxygen species, presumably originating from both inside and outside the mitochondria. In the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of PD, time‐course experiments suggest that oxidative stress is an early event that may directly kill some of the dopaminergic neurons. In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. If correct, this may be a reason why neuroprotective trials using a single agent, such as an antioxidant, have thus far generated disappointing results.
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DOI: 10.1196/annals.1427.023
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Typically PD is a sporadic neurological disorder, and over time affected patients see their disability growing and their quality of life declining. Oxidative stress has been hypothesized to be linked to both the initiation and the progression of PD. Preclinical findings from both in vitro and in vivo experimental models of PD suggest that the neurodegenerative process starts with otherwise healthy neurons being hit by some etiological factors, which sets into motion a cascade of deleterious events. In these models initial molecular alterations in degenerating dopaminergic neurons include increased formation of reactive oxygen species, presumably originating from both inside and outside the mitochondria. In the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of PD, time‐course experiments suggest that oxidative stress is an early event that may directly kill some of the dopaminergic neurons. In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. If correct, this may be a reason why neuroprotective trials using a single agent, such as an antioxidant, have thus far generated disappointing results.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Chun Zhou</name><affiliations><json:string>Department of Neurology</json:string></affiliations></json:item><json:item><name>Yong Huang</name><affiliations><json:string>Department of Neurology</json:string></affiliations></json:item><json:item><name>Serge Przedborski</name><affiliations><json:string>Department of Neurology</json:string><json:string>Departments of Pathology and Cell Biology, Columbia University, New York, New York, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>oxidative stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>reactive oxygen species</value></json:item></subject><articleId><json:string>NYAS1147023</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson's disease (PD) is a common adult‐onset neurodegenerative disorder. 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In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. 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In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. If correct, this may be a reason why neuroprotective trials using a single agent, such as an antioxidant, have thus far generated disappointing results.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>oxidative stress</term></item><item><term>reactive oxygen species</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/81C7E6C306D3A01532E0D629789054A211CA11B3/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 Inc</publisherName><publisherLoc>Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="12001"><doi origin="wiley">10.1196/nyas.2008.1147.issue-1</doi><titleGroup><title type="main">Mitochondria and Oxidative Stress in Neurodegenerative Disorders</title></titleGroup><numberingGroup><numbering type="journalVolume" number="1147">1147</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2008-12">December 2008</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="10" status="forIssue"><doi origin="wiley">10.1196/annals.1427.023</doi><idGroup><id type="unit" value="NYAS1147023"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">Part III. Evidence for Oxidant Damage in Brains</title></titleGroup><copyright>© 2008 New York Academy of Sciences</copyright><eventGroup><event type="firstOnline" date="2008-12-08"></event><event type="publishedOnlineFinalForm" date="2008-12-08"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.5 mode:FullText source:FullText result:FullText" date="2010-04-06"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="93">93</numbering><numbering type="pageLast" number="104">104</numbering></numberingGroup><correspondenceTo>Address for correspondence: Dr. Serge Przedborski, BB‐302, Columbia University Medical Center, 650 West 168th Street, New York, NY 10032. Voice: +212‐342‐4119; fax: +212‐342‐3663. <email>SP30@Columbia.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS1147023.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="104"></count><count type="linksCrossRef" number="90"></count></countGroup><titleGroup><title type="main">Oxidative Stress in Parkinson's Disease</title><title type="subtitle">A Mechanism of Pathogenic and Therapeutic Significance</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Chun</givenNames><familyName>Zhou</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Yong</givenNames><familyName>Huang</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2"><personName><givenNames>Serge</givenNames><familyName>Przedborski</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Neurology</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Departments of Pathology and Cell Biology, Columbia University, New York, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">oxidative stress</keyword><keyword xml:id="k3">reactive oxygen species</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinson's disease (PD) is a common adult‐onset neurodegenerative disorder. Typically PD is a sporadic neurological disorder, and over time affected patients see their disability growing and their quality of life declining. Oxidative stress has been hypothesized to be linked to both the initiation and the progression of PD. Preclinical findings from both <i>in vitro</i> and <i>in vivo</i> experimental models of PD suggest that the neurodegenerative process starts with otherwise healthy neurons being hit by some etiological factors, which sets into motion a cascade of deleterious events. In these models initial molecular alterations in degenerating dopaminergic neurons include increased formation of reactive oxygen species, presumably originating from both inside and outside the mitochondria. In the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of PD, time‐course experiments suggest that oxidative stress is an early event that may directly kill some of the dopaminergic neurons. In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. 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Typically PD is a sporadic neurological disorder, and over time affected patients see their disability growing and their quality of life declining. Oxidative stress has been hypothesized to be linked to both the initiation and the progression of PD. Preclinical findings from both in vitro and in vivo experimental models of PD suggest that the neurodegenerative process starts with otherwise healthy neurons being hit by some etiological factors, which sets into motion a cascade of deleterious events. In these models initial molecular alterations in degenerating dopaminergic neurons include increased formation of reactive oxygen species, presumably originating from both inside and outside the mitochondria. In the 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) mouse model of PD, time‐course experiments suggest that oxidative stress is an early event that may directly kill some of the dopaminergic neurons. In this model it seems that oxidative stress may play a greater role in the demise of dopaminergic neurons indirectly by activating intracellular, cell death‐related, molecular pathways. As the neurodegenerative process evolves in the MPTP mouse model, indices of neuroinflammation develop, such as microglial activation. The latter increases the level of oxidative stress to which the neighboring compromised neurons are subjected to, thereby promoting their demise. However, these experimental studies have also shown that oxidative stress is not the sole deleterious factor implicated in the death of dopaminergic neurons. Should a similar multifactorial cascade underlie dopaminergic neuron degeneration in PD, then the optimal therapy for this disease may have to rely on a cocktail of agents, each targeting a different critical component of this hypothesized pathogenic cascade. If correct, this may be a reason why neuroprotective trials using a single agent, such as an antioxidant, have thus far generated disappointing results.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>oxidative stress</topic><topic>reactive oxygen species</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of SciencesMitochondria and Oxidative Stress in Neurodegenerative Disorders</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>1147</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>93</start><end>104</end><total>12</total></extent></part></relatedItem><identifier type="istex">81C7E6C306D3A01532E0D629789054A211CA11B3</identifier><identifier type="DOI">10.1196/annals.1427.023</identifier><identifier type="ArticleID">NYAS1147023</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2008 New York Academy of Sciences</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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