Alterations of striatal neurons in benign hereditary chorea
Identifieur interne : 003126 ( Istex/Corpus ); précédent : 003125; suivant : 003127Alterations of striatal neurons in benign hereditary chorea
Auteurs : Galit Kleiner-Fisman ; Noel Y. Calingasan ; Mary Putt ; June Chen ; M. Flint Beal ; Anthony E. LangSource :
- Movement Disorders [ 0885-3185 ] ; 2005-10.
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- KwdEn :
Abstract
Benign hereditary chorea (BHC) recently has been associated with mutations in TITF‐1 gene, although a pathological study of an individual with BHC and a TITF‐1 mutation revealed no significant gross or microscopic abnormalities using standard methods. Immunohistochemical staining of striatal tissue from a BHC‐affected postmortem brain was performed using antibodies against neurotransmitters of interneurons whose tangential migration is mediated by TITF‐1. There was a loss of most TITF‐1–mediated striatal interneurons in the BHC specimen compared to four matched control brains. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20577
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ISTEX:93B807CB7E16134EA05B9026D8B2B230655481A7Le document en format XML
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Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. Lang</name><affiliation><mods:affiliation>The Morton and Gloria Shulman Movement Disorders Center, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-10">2005-10</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1353">1353</biblScope><biblScope unit="page" to="1357">1357</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">93B807CB7E16134EA05B9026D8B2B230655481A7</idno><idno type="DOI">10.1002/mds.20577</idno><idno type="ArticleID">MDS20577</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>TITF‐1</term><term>benign hereditary chorea</term><term>migration</term><term>pathology</term><term>projection neurons</term><term>striatal interneurons</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Benign hereditary chorea (BHC) recently has been associated with mutations in TITF‐1 gene, although a pathological study of an individual with BHC and a TITF‐1 mutation revealed no significant gross or microscopic abnormalities using standard methods. Immunohistochemical staining of striatal tissue from a BHC‐affected postmortem brain was performed using antibodies against neurotransmitters of interneurons whose tangential migration is mediated by TITF‐1. There was a loss of most TITF‐1–mediated striatal interneurons in the BHC specimen compared to four matched control brains. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Galit Kleiner‐Fisman MD</name><affiliations><json:string>Parkinson's Disease Research, Education and Clinical Center (PADRECC), Philadelphia VA Hospital, Philadelphia, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>Noel Y. Calingasan PhD</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Mary Putt PhD</name><affiliations><json:string>Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</json:string></affiliations></json:item><json:item><name>June Chen MA</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>M.Flint Beal MD</name><affiliations><json:string>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</json:string></affiliations></json:item><json:item><name>Anthony E. Lang MD</name><affiliations><json:string>The Morton and Gloria Shulman Movement Disorders Center, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>benign hereditary chorea</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>pathology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>striatal interneurons</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>projection neurons</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>TITF‐1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>migration</value></json:item></subject><language><json:string>eng</json:string></language><abstract>Benign hereditary chorea (BHC) recently has been associated with mutations in TITF‐1 gene, although a pathological study of an individual with BHC and a TITF‐1 mutation revealed no significant gross or microscopic abnormalities using standard methods. Immunohistochemical staining of striatal tissue from a BHC‐affected postmortem brain was performed using antibodies against neurotransmitters of interneurons whose tangential migration is mediated by TITF‐1. 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Y.</givenNames><familyName>Calingasan</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Mary</givenNames><familyName>Putt</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>June</givenNames><familyName>Chen</familyName><degrees>MA</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>M.Flint</givenNames><familyName>Beal</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Anthony E.</givenNames><familyName>Lang</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Parkinson's Disease Research, Education and Clinical Center (PADRECC), Philadelphia VA Hospital, Philadelphia, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="CA" type="organization"><unparsedAffiliation>The Morton and Gloria Shulman Movement Disorders Center, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">benign hereditary chorea</keyword><keyword xml:id="kwd2">pathology</keyword><keyword xml:id="kwd3">striatal interneurons</keyword><keyword xml:id="kwd4">projection neurons</keyword><keyword xml:id="kwd5">TITF‐1</keyword><keyword xml:id="kwd6">migration</keyword></keywordGroup><fundingInfo><fundingAgency>Huntington's Society of America</fundingAgency><fundingNumber>NS39258</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Hereditary Disease Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>National Parkinson Foundation (Miami, FL)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Mayvon Foundation (Toronto, ON, Canada)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Elizabeth Barford Scholarship at the University Health Network, Toronto, Canada</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Benign hereditary chorea (BHC) recently has been associated with mutations in TITF‐1 gene, although a pathological study of an individual with BHC and a TITF‐1 mutation revealed no significant gross or microscopic abnormalities using standard methods. Immunohistochemical staining of striatal tissue from a BHC‐affected postmortem brain was performed using antibodies against neurotransmitters of interneurons whose tangential migration is mediated by TITF‐1. There was a loss of most TITF‐1–mediated striatal interneurons in the BHC specimen compared to four matched control brains. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Alterations of striatal neurons in benign hereditary chorea</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Pathology of BHC</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Alterations of striatal neurons in benign hereditary chorea</title></titleInfo><name type="personal"><namePart type="given">Galit</namePart><namePart type="family">Kleiner‐Fisman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson's Disease Research, Education and Clinical Center (PADRECC), Philadelphia VA Hospital, Philadelphia, Pennsylvania, USA</affiliation><description>Correspondence: University of Pennsylvania, PADRECC, Philadelphia Veterans Administration Hospital, 3900 Woodland Avenue, Philadelphia, PA, 19104</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Noel Y.</namePart><namePart type="family">Calingasan</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mary</namePart><namePart type="family">Putt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Biostatistics and Epidemiology, University of Pennsylvania, Philadelphia, Pennsylvania, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">June</namePart><namePart type="family">Chen</namePart><namePart type="termsOfAddress">MA</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.Flint</namePart><namePart type="family">Beal</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anthony E.</namePart><namePart type="family">Lang</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>The Morton and Gloria Shulman Movement Disorders Center, Toronto Western Hospital, University of Toronto, Toronto, Ontario, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-10</dateIssued><dateCaptured encoding="w3cdtf">2004-06-29</dateCaptured><dateValid encoding="w3cdtf">2005-01-31</dateValid><copyrightDate encoding="w3cdtf">2005</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">2</extent><extent unit="tables">1</extent><extent unit="references">10</extent><extent unit="words">2507</extent></physicalDescription><abstract lang="en">Benign hereditary chorea (BHC) recently has been associated with mutations in TITF‐1 gene, although a pathological study of an individual with BHC and a TITF‐1 mutation revealed no significant gross or microscopic abnormalities using standard methods. Immunohistochemical staining of striatal tissue from a BHC‐affected postmortem brain was performed using antibodies against neurotransmitters of interneurons whose tangential migration is mediated by TITF‐1. There was a loss of most TITF‐1–mediated striatal interneurons in the BHC specimen compared to four matched control brains. © 2005 Movement Disorder Society</abstract><note type="funding">Huntington's Society of America - No. NS39258; </note><note type="funding">Hereditary Disease Foundation</note><note type="funding">National Parkinson Foundation (Miami, FL)</note><note type="funding">Mayvon Foundation (Toronto, ON, Canada)</note><note type="funding">Elizabeth Barford Scholarship at the University Health Network, Toronto, Canada</note><subject lang="en"><genre>Keywords</genre><topic>benign hereditary chorea</topic><topic>pathology</topic><topic>striatal interneurons</topic><topic>projection neurons</topic><topic>TITF‐1</topic><topic>migration</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1353</start><end>1357</end><total>5</total></extent></part></relatedItem><identifier type="istex">93B807CB7E16134EA05B9026D8B2B230655481A7</identifier><identifier type="DOI">10.1002/mds.20577</identifier><identifier type="ArticleID">MDS20577</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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