Lewy body pathology in fetal grafts
Identifieur interne : 002687 ( Main/Corpus ); précédent : 002686; suivant : 002688Lewy body pathology in fetal grafts
Auteurs : Yaping Chu ; Jeffrey H. KordowerSource :
- Annals of the New York Academy of SciencesThe Year in Neurology 2 [ 0077-8923 ] ; 2010-01.
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Abstract
Although fetal nigral transplants have been shown to survive grafting into the striatum, increased [18F]6‐fluroro‐l‐3,4‐dihydroxyphenylalanine (18F‐DOPA) uptake and improved motor function in open‐label assessments have failed to establish any clinical benefits in double‐blind, sham‐controlled studies. To understand morphological and neurochemical alterations of grafted neurons, we performed postmortem analyses on six Parkinson's disease (PD) patients who had received fetal tissue transplantation 18–19 months, 4 years, and 14 years previously. These studies revealed robust neuronal survival with normal dopaminergic phenotypes in 18‐month‐old grafts and decreased dopamine transporter and increased cytoplasmic α‐synuclein in 4‐year‐old grafts. We also found a decline of both dopamine transporter and tyrosine hydroxylase and the formation of Lewy body–like inclusions in 14‐year‐old grafts, which stained positive for α‐synuclein and ubiquitin proteins. These pathological changes suggest that PD is an ongoing process that affects grafted cells in the striatum in a manner similar to how resident dopamine neurons are affected in the substantia nigra.
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DOI: 10.1111/j.1749-6632.2009.05229.x
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To understand morphological and neurochemical alterations of grafted neurons, we performed postmortem analyses on six Parkinson's disease (PD) patients who had received fetal tissue transplantation 18–19 months, 4 years, and 14 years previously. These studies revealed robust neuronal survival with normal dopaminergic phenotypes in 18‐month‐old grafts and decreased dopamine transporter and increased cytoplasmic α‐synuclein in 4‐year‐old grafts. We also found a decline of both dopamine transporter and tyrosine hydroxylase and the formation of Lewy body–like inclusions in 14‐year‐old grafts, which stained positive for α‐synuclein and ubiquitin proteins. 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To understand morphological and neurochemical alterations of grafted neurons, we performed postmortem analyses on six Parkinson's disease (PD) patients who had received fetal tissue transplantation 18–19 months, 4 years, and 14 years previously. These studies revealed robust neuronal survival with normal dopaminergic phenotypes in 18‐month‐old grafts and decreased dopamine transporter and increased cytoplasmic α‐synuclein in 4‐year‐old grafts. We also found a decline of both dopamine transporter and tyrosine hydroxylase and the formation of Lewy body–like inclusions in 14‐year‐old grafts, which stained positive for α‐synuclein and ubiquitin proteins. 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Voice: 312‐563‐3570; fax: 312‐563‐3571. <email>jkordowe@rush.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS5229.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="9"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="63"></count><count type="linksCrossRef" number="69"></count></countGroup><titleGroup><title type="main">Lewy body pathology in fetal grafts</title><title type="shortAuthors">Chu & Kordower</title><title type="short">Lewy body pathology in fetal grafts</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Yaping</givenNames><familyName>Chu</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Jeffrey H.</givenNames><familyName>Kordower</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="US"><unparsedAffiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">fetal tissue transplantation</keyword><keyword xml:id="k2">Parkinson's disease</keyword><keyword xml:id="k3">dopaminergic phenotype</keyword><keyword xml:id="k4">α‐synuclein</keyword><keyword xml:id="k5">ubiquitin</keyword><keyword xml:id="k6">thioflavin‐s</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Although fetal nigral transplants have been shown to survive grafting into the striatum, increased [<sup>18</sup>F]6‐fluroro‐<sc>l</sc>‐3,4‐dihydroxyphenylalanine (<sup>18</sup>F‐DOPA) uptake and improved motor function in open‐label assessments have failed to establish any clinical benefits in double‐blind, sham‐controlled studies. To understand morphological and neurochemical alterations of grafted neurons, we performed postmortem analyses on six Parkinson's disease (PD) patients who had received fetal tissue transplantation 18–19 months, 4 years, and 14 years previously. These studies revealed robust neuronal survival with normal dopaminergic phenotypes in 18‐month‐old grafts and decreased dopamine transporter and increased cytoplasmic α‐synuclein in 4‐year‐old grafts. We also found a decline of both dopamine transporter and tyrosine hydroxylase and the formation of Lewy body–like inclusions in 14‐year‐old grafts, which stained positive for α‐synuclein and ubiquitin proteins. These pathological changes suggest that PD is an ongoing process that affects grafted cells in the striatum in a manner similar to how resident dopamine neurons are affected in the substantia nigra.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Lewy body pathology in fetal grafts</title></titleInfo><titleInfo type="abbreviated"><title>Lewy body pathology in fetal grafts</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Lewy body pathology in fetal grafts</title></titleInfo><name type="personal"><namePart type="given">Yaping</namePart><namePart type="family">Chu</namePart><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffrey H.</namePart><namePart type="family">Kordower</namePart><affiliation>Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Inc</publisher><place><placeTerm type="text">Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2010-01</dateIssued><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">9</extent><extent unit="references">63</extent></physicalDescription><abstract lang="en">Although fetal nigral transplants have been shown to survive grafting into the striatum, increased [18F]6‐fluroro‐l‐3,4‐dihydroxyphenylalanine (18F‐DOPA) uptake and improved motor function in open‐label assessments have failed to establish any clinical benefits in double‐blind, sham‐controlled studies. To understand morphological and neurochemical alterations of grafted neurons, we performed postmortem analyses on six Parkinson's disease (PD) patients who had received fetal tissue transplantation 18–19 months, 4 years, and 14 years previously. These studies revealed robust neuronal survival with normal dopaminergic phenotypes in 18‐month‐old grafts and decreased dopamine transporter and increased cytoplasmic α‐synuclein in 4‐year‐old grafts. We also found a decline of both dopamine transporter and tyrosine hydroxylase and the formation of Lewy body–like inclusions in 14‐year‐old grafts, which stained positive for α‐synuclein and ubiquitin proteins. These pathological changes suggest that PD is an ongoing process that affects grafted cells in the striatum in a manner similar to how resident dopamine neurons are affected in the substantia nigra.</abstract><subject lang="en"><genre>Keywords</genre><topic>fetal tissue transplantation</topic><topic>Parkinson's disease</topic><topic>dopaminergic phenotype</topic><topic>α‐synuclein</topic><topic>ubiquitin</topic><topic>thioflavin‐s</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of SciencesThe Year in Neurology 2</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>ANNALS OF THE NEW YORK ACADEMY OF SCIENCES</topic></subject><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>2010</date><detail type="volume"><caption>vol.</caption><number>1184</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>55</start><end>67</end><total>13</total></extent></part></relatedItem><identifier type="istex">D2C43544C6E37AFFAB7C6B55506B800882C6EA2B</identifier><identifier type="DOI">10.1111/j.1749-6632.2009.05229.x</identifier><identifier type="ArticleID">NYAS5229</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 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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