Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model
Identifieur interne : 001401 ( Main/Corpus ); précédent : 001400; suivant : 001402Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model
Auteurs : René Hernández- Vargas ; Luis Fonseca- Ornelas ; Ignacio L Pez- González ; Juan Riesgo- Escovar ; Mario Zurita ; Enrique ReynaudSource :
- genesis [ 1526-954X ] ; 2011-05.
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Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disorder in humans. It affects 1% of the population over 65‐years old. Its causes are environmental and genetic. As the world population ages, there is an urgent need for better and more detailed animal models for this kind of disease. In this work we show that the use of transgenic Drosophila is comparable to more complicated and costly animal models such as mice. The Drosophila model behaves very similar to the equivalent transgenic mice model. We show that both Synphilin‐1 and α‐synuclein are toxic by themselves, but when co‐expressed, they suppress their toxicity reciprocally. Importantly, the symptoms induced in the fly can be treated and partially reverted using standard PD pharmacological treatments. This work showcases Drosophila as a detailed and multifaceted model for Parkinson's disease, providing a convenient platform in which to study and find new genetic modifiers of PD. genesis 49:392–402, 2011. © 2011 Wiley‐Liss, Inc.
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DOI: 10.1002/dvg.20740
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ISTEX:422509D73063BA42E12C834111AAF272F7C3E0C7Le document en format XML
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It affects 1% of the population over 65‐years old. Its causes are environmental and genetic. As the world population ages, there is an urgent need for better and more detailed animal models for this kind of disease. In this work we show that the use of transgenic Drosophila is comparable to more complicated and costly animal models such as mice. The Drosophila model behaves very similar to the equivalent transgenic mice model. We show that both Synphilin‐1 and α‐synuclein are toxic by themselves, but when co‐expressed, they suppress their toxicity reciprocally. Importantly, the symptoms induced in the fly can be treated and partially reverted using standard PD pharmacological treatments. This work showcases Drosophila as a detailed and multifaceted model for Parkinson's disease, providing a convenient platform in which to study and find new genetic modifiers of PD. genesis 49:392–402, 2011. © 2011 Wiley‐Liss, Inc.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>René Hernández‐ Vargas</name><affiliations><json:string>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</json:string></affiliations></json:item><json:item><name>Luis Fonseca‐ Ornelas</name><affiliations><json:string>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</json:string></affiliations></json:item><json:item><name>Ignacio López‐ González</name><affiliations><json:string>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</json:string></affiliations></json:item><json:item><name>Juan Riesgo‐ Escovar</name><affiliations><json:string>Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Campus UNAM‐Juriquilla, Universidad Nacional Autónoma de México, Querétaro, México</json:string></affiliations></json:item><json:item><name>Mario Zurita</name><affiliations><json:string>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</json:string></affiliations></json:item><json:item><name>Enrique Reynaud</name><affiliations><json:string>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>neurodegenerative disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>amyloid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>animal model</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lewy bodies</value></json:item></subject><articleId><json:string>DVG20740</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson's disease (PD) is the second most common neurodegenerative disorder in humans. 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This work showcases Drosophila as a detailed and multifaceted model for Parkinson's disease, providing a convenient platform in which to study and find new genetic modifiers of PD. genesis 49:392–402, 2011. © 2011 Wiley‐Liss, Inc.</abstract><qualityIndicators><score>6.872</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1016</abstractCharCount><pdfWordCount>5691</pdfWordCount><pdfCharCount>37576</pdfCharCount><pdfPageCount>11</pdfPageCount><abstractWordCount>156</abstractWordCount></qualityIndicators><title>Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model</title><genre><json:string>article</json:string></genre><host><volume>49</volume><publisherId><json:string>DVG</json:string></publisherId><pages><total>10</total><last>402</last><first>392</first></pages><issn><json:string>1526-954X</json:string></issn><issue>5</issue><subject><json:item><value>Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1526-968X</json:string></eissn><title>genesis</title><doi><json:string>10.1002/(ISSN)1526-968X</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/dvg.20740</json:string></doi><id>422509D73063BA42E12C834111AAF272F7C3E0C7</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/422509D73063BA42E12C834111AAF272F7C3E0C7/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/422509D73063BA42E12C834111AAF272F7C3E0C7/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/422509D73063BA42E12C834111AAF272F7C3E0C7/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note>DGAPA/UNAM - No. IN211707; 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bodies</keyword></keywordGroup><fundingInfo><fundingAgency>DGAPA/UNAM</fundingAgency><fundingNumber>IN211707</fundingNumber><fundingNumber>IX209904</fundingNumber><fundingNumber>IN216507</fundingNumber><fundingNumber>IN217210</fundingNumber></fundingInfo><fundingInfo><fundingAgency>CONACyT</fundingAgency><fundingNumber>J36866‐N</fundingNumber><fundingNumber>84362</fundingNumber><fundingNumber>269435</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease (PD) is the second most common neurodegenerative disorder in humans. It affects 1% of the population over 65‐years old. Its causes are environmental and genetic. As the world population ages, there is an urgent need for better and more detailed animal models for this kind of disease. In this work we show that the use of transgenic <i>Drosophila</i> is comparable to more complicated and costly animal models such as mice. The <i>Drosophila</i> model behaves very similar to the equivalent transgenic mice model. We show that both Synphilin‐1 and α‐synuclein are toxic by themselves, but when co‐expressed, they suppress their toxicity reciprocally. Importantly, the symptoms induced in the fly can be treated and partially reverted using standard PD pharmacological treatments. This work showcases <i>Drosophila</i> as a detailed and multifaceted model for Parkinson's disease, providing a convenient platform in which to study and find new genetic modifiers of PD. genesis 49:392–402, 2011. © 2011 Wiley‐Liss, Inc.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Synphilin‐1 and Alpha‐Synuclein</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Synphilin suppresses α‐synuclein neurotoxicity in a Parkinson's disease Drosophila model</title></titleInfo><name type="personal"><namePart type="given">René Hernández‐</namePart><namePart type="family">Vargas</namePart><affiliation>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Luis Fonseca‐</namePart><namePart type="family">Ornelas</namePart><affiliation>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ignacio López‐</namePart><namePart type="family">González</namePart><affiliation>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Juan Riesgo‐</namePart><namePart type="family">Escovar</namePart><affiliation>Departamento de Neurobiología del Desarrollo y Neurofisiología, Instituto de Neurobiología, Campus UNAM‐Juriquilla, Universidad Nacional Autónoma de México, Querétaro, México</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mario</namePart><namePart type="family">Zurita</namePart><affiliation>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Enrique</namePart><namePart type="family">Reynaud</namePart><affiliation>Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México, Cuernavaca, México</affiliation><description>Correspondence: Instituto de Biotecnología, UNAM, A.P. 510‐3, Cuernavaca, Mor., 62210 México</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2010-08-24</dateCaptured><dateValid encoding="w3cdtf">2011-02-13</dateValid><copyrightDate encoding="w3cdtf">2011</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">4</extent><extent unit="references">74</extent><extent unit="words">5504</extent></physicalDescription><abstract lang="en">Parkinson's disease (PD) is the second most common neurodegenerative disorder in humans. It affects 1% of the population over 65‐years old. Its causes are environmental and genetic. As the world population ages, there is an urgent need for better and more detailed animal models for this kind of disease. In this work we show that the use of transgenic Drosophila is comparable to more complicated and costly animal models such as mice. The Drosophila model behaves very similar to the equivalent transgenic mice model. We show that both Synphilin‐1 and α‐synuclein are toxic by themselves, but when co‐expressed, they suppress their toxicity reciprocally. Importantly, the symptoms induced in the fly can be treated and partially reverted using standard PD pharmacological treatments. This work showcases Drosophila as a detailed and multifaceted model for Parkinson's disease, providing a convenient platform in which to study and find new genetic modifiers of PD. genesis 49:392–402, 2011. © 2011 Wiley‐Liss, Inc.</abstract><note type="funding">DGAPA/UNAM - No. IN211707; No. IX209904; No. IN216507; No. IN217210; </note><note type="funding">CONACyT - No. J36866‐N; No. 84362; No. 269435; </note><subject lang="en"><genre>Keywords</genre><topic>neurodegenerative disease</topic><topic>amyloid</topic><topic>animal model</topic><topic>Lewy bodies</topic></subject><relatedItem type="host"><titleInfo><title>genesis</title></titleInfo><titleInfo type="abbreviated"><title>Genesis</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">1526-954X</identifier><identifier type="eISSN">1526-968X</identifier><identifier type="DOI">10.1002/(ISSN)1526-968X</identifier><identifier type="PublisherID">DVG</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>392</start><end>402</end><total>10</total></extent></part></relatedItem><relatedItem type="preceding"><titleInfo><title>Developmental Genetics</title></titleInfo><identifier type="ISSN">0192-253X</identifier><part><date point="end">1999</date><detail type="volume"><caption>last vol.</caption><number>25</number></detail><detail type="issue"><caption>last no.</caption><number>4</number></detail></part></relatedItem><identifier type="istex">422509D73063BA42E12C834111AAF272F7C3E0C7</identifier><identifier type="DOI">10.1002/dvg.20740</identifier><identifier type="ArticleID">DVG20740</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Wiley‐Liss, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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