Presynaptic monoaminergic vesicles in Parkinson's disease and normal aging
Identifieur interne : 001C22 ( Main/Corpus ); précédent : 001C21; suivant : 001C23Presynaptic monoaminergic vesicles in Parkinson's disease and normal aging
Auteurs : Frey ; Robert A. Koeppe ; Michael R. Kilbourn ; Thierry M. Vander Borght ; Roger L. Albin ; Sid Gilman ; David E. KuhlSource :
- Annals of Neurology [ 0364-5134 ] ; 1996-12.
Abstract
We present development and human application of a method for determining the regional cerebral density of the type 2 vesicular monoamine transporter (VMAT2) using positron emission tomography (PET) and [11C]dihydrotetrabenazine (DTBZ). Previous animal studies indicate striatal VMAT2 density is linearly related to the integrity of substantia nigra dopamine neurons and is not subject to drug‐or lesion‐compensatory regulation. In the present studies, kinetic compartmental modeling was employed to estimate blood‐brain [11C]DTBZ transport (K1,) and VMAT2 binding site density (tissue‐to‐plasma DTBZ distribution volume, DV)from the cerebral and plasma DTBZ time courses her intravenous tracer injection. In controls, we found reductions of putamen DTBZ DV with advancing age, corresponding to losses of 0.77% per year in specific VMAT2 binding. Parkinson's disease (PD) patients had reduction in specific DTBZ DV in the putamen (−61%) and in the caudate nucleus (−43%). There was no overlap of lowest specific putamen DTBZ DV between individual elderly controls and PD patients. The present results indicate the suitability of [11C]DTBZ PET for objective quantification of nigrostriatal integrity, including evaluation of PD progression and its possible therapeutic modification.
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DOI: 10.1002/ana.410400609
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Previous animal studies indicate striatal VMAT2 density is linearly related to the integrity of substantia nigra dopamine neurons and is not subject to drug‐or lesion‐compensatory regulation. In the present studies, kinetic compartmental modeling was employed to estimate blood‐brain [11C]DTBZ transport (K1,) and VMAT2 binding site density (tissue‐to‐plasma DTBZ distribution volume, DV)from the cerebral and plasma DTBZ time courses her intravenous tracer injection. In controls, we found reductions of putamen DTBZ DV with advancing age, corresponding to losses of 0.77% per year in specific VMAT2 binding. Parkinson's disease (PD) patients had reduction in specific DTBZ DV in the putamen (−61%) and in the caudate nucleus (−43%). There was no overlap of lowest specific putamen DTBZ DV between individual elderly controls and PD patients. The present results indicate the suitability of [11C]DTBZ PET for objective quantification of nigrostriatal integrity, including evaluation of PD progression and its possible therapeutic modification.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Frey MD, PhD</name><affiliations><json:string>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</json:string><json:string>Departments of Neurology, University of Michigan, Ann Arbor, MI</json:string><json:string>Departments of Mental Health Research Institute, University of Michigan, Ann Arbor, MI</json:string></affiliations></json:item><json:item><name>Robert A. Koeppe PhD</name><affiliations><json:string>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</json:string></affiliations></json:item><json:item><name>Michael R. 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Previous animal studies indicate striatal VMAT2 density is linearly related to the integrity of substantia nigra dopamine neurons and is not subject to drug‐or lesion‐compensatory regulation. In the present studies, kinetic compartmental modeling was employed to estimate blood‐brain [11C]DTBZ transport (K1,) and VMAT2 binding site density (tissue‐to‐plasma DTBZ distribution volume, DV)from the cerebral and plasma DTBZ time courses her intravenous tracer injection. In controls, we found reductions of putamen DTBZ DV with advancing age, corresponding to losses of 0.77% per year in specific VMAT2 binding. Parkinson's disease (PD) patients had reduction in specific DTBZ DV in the putamen (−61%) and in the caudate nucleus (−43%). There was no overlap of lowest specific putamen DTBZ DV between individual elderly controls and PD patients. The present results indicate the suitability of [11C]DTBZ PET for objective quantification of nigrostriatal integrity, including evaluation of PD progression and its possible therapeutic modification.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-02-01">Received</change><change when="1996-05-31">Registration</change><change when="1996-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/B3721161C2002D3E92CABCA5FFFCBE7B7169225F/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" 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Aging</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2 #af3" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Kirk A.</givenNames><familyName>Frey</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Robert A.</givenNames><familyName>Koeppe</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael R.</givenNames><familyName>Kilbourn</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Thierry M.</givenNames><familyName>Vander Borght</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Roger L.</givenNames><familyName>Albin</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Sid</givenNames><familyName>Gilman</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>David E.</givenNames><familyName>Kuhl</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Departments of Neurology, University of Michigan, Ann Arbor, MI</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Departments of Mental Health Research Institute, University of Michigan, Ann Arbor, MI</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We present development and human application of a method for determining the regional cerebral density of the type 2 vesicular monoamine transporter (VMAT2) using positron emission tomography (PET) and [<sup>11</sup>C]dihydrotetrabenazine (DTBZ). Previous animal studies indicate striatal VMAT2 density is linearly related to the integrity of substantia nigra dopamine neurons and is not subject to drug‐or lesion‐compensatory regulation. In the present studies, kinetic compartmental modeling was employed to estimate blood‐brain [<sup>11</sup>C]DTBZ transport (<i>K</i><sub>1</sub>,) and VMAT2 binding site density (tissue‐to‐plasma DTBZ distribution volume, <i>DV</i>)from the cerebral and plasma DTBZ time courses her intravenous tracer injection. In controls, we found reductions of putamen DTBZ <i>DV</i> with advancing age, corresponding to losses of 0.77% per year in specific VMAT2 binding. Parkinson's disease (PD) patients had reduction in specific DTBZ <i>DV</i> in the putamen (−61%) and in the caudate nucleus (−43%). There was no overlap of lowest specific putamen DTBZ <i>DV</i> between individual elderly controls and PD patients. The present results indicate the suitability of [<sup>11</sup>C]DTBZ PET for objective quantification of nigrostriatal integrity, including evaluation of PD progression and its possible therapeutic modification.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Presynaptic monoaminergic vesicles in Parkinson's disease and normal aging</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>[11]DTBZ PET in PD and Aging</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Presynaptic monoaminergic vesicles in Parkinson's disease and normal aging</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Frey</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</affiliation><affiliation>Departments of Neurology, University of Michigan, Ann Arbor, MI</affiliation><affiliation>Departments of Mental Health Research Institute, University of Michigan, Ann Arbor, MI</affiliation><description>Correspondence: The University of Michigan Hospitals, B1G 412/0028 AGH, 1500 East Medical Center Drive, Ann Arbor, MI 48109‐0028</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert A.</namePart><namePart type="family">Koeppe</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael R.</namePart><namePart type="family">Kilbourn</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thierry M.</namePart><namePart type="family">Vander Borght</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Internal Medicine (Division of Nuclear Medicine), University of Michigan, Ann Arbor, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roger L.</namePart><namePart type="family">Albin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Neurology, University of Michigan, Ann Arbor, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sid</namePart><namePart type="family">Gilman</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Neurology, University of Michigan, Ann Arbor, MI</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David E.</namePart><namePart type="family">Kuhl</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Departments of Neurology, University of Michigan, Ann Arbor, MI</affiliation><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">1996-12</dateIssued><dateCaptured encoding="w3cdtf">1996-02-01</dateCaptured><dateValid encoding="w3cdtf">1996-05-31</dateValid><copyrightDate encoding="w3cdtf">1996</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">6</extent><extent unit="tables">3</extent><extent unit="references">66</extent></physicalDescription><abstract lang="en">We present development and human application of a method for determining the regional cerebral density of the type 2 vesicular monoamine transporter (VMAT2) using positron emission tomography (PET) and [11C]dihydrotetrabenazine (DTBZ). Previous animal studies indicate striatal VMAT2 density is linearly related to the integrity of substantia nigra dopamine neurons and is not subject to drug‐or lesion‐compensatory regulation. In the present studies, kinetic compartmental modeling was employed to estimate blood‐brain [11C]DTBZ transport (K1,) and VMAT2 binding site density (tissue‐to‐plasma DTBZ distribution volume, DV)from the cerebral and plasma DTBZ time courses her intravenous tracer injection. In controls, we found reductions of putamen DTBZ DV with advancing age, corresponding to losses of 0.77% per year in specific VMAT2 binding. Parkinson's disease (PD) patients had reduction in specific DTBZ DV in the putamen (−61%) and in the caudate nucleus (−43%). There was no overlap of lowest specific putamen DTBZ DV between individual elderly controls and PD patients. The present results indicate the suitability of [11C]DTBZ PET for objective quantification of nigrostriatal integrity, including evaluation of PD progression and its possible therapeutic modification.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>873</start><end>884</end><total>12</total></extent></part></relatedItem><identifier type="istex">B3721161C2002D3E92CABCA5FFFCBE7B7169225F</identifier><identifier type="DOI">10.1002/ana.410400609</identifier><identifier type="ArticleID">ANA410400609</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1996 American Neurological Association</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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