Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins
Identifieur interne : 001063 ( Istex/Corpus ); précédent : 001062; suivant : 001064Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins
Auteurs : Patrick Vermersch ; Patrick Delacourte ; France Javoy-Agid ; Jean-Jacques Hauw ; Yves AgidSource :
- Annals of Neurology [ 0364-5134 ] ; 1993-05.
Abstract
In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.
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DOI: 10.1002/ana.410330506
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins</title><author><name sortKey="Vermersch, Patrick" sort="Vermersch, Patrick" uniqKey="Vermersch P" first="Patrick" last="Vermersch">Patrick Vermersch</name><affiliation><mods:affiliation>Unité INSERM 156, Lille</mods:affiliation></affiliation></author><author><name sortKey="Delacourte, Patrick" sort="Delacourte, Patrick" uniqKey="Delacourte P" first="Patrick" last="Delacourte">Patrick Delacourte</name><affiliation><mods:affiliation>Unité INSERM 156, Lille</mods:affiliation></affiliation><affiliation><mods:affiliation>Unité INSERM 156, Place de Verdun, 59045 Lille cedex, France</mods:affiliation></affiliation></author><author><name sortKey="Javoy Gid, France" sort="Javoy Gid, France" uniqKey="Javoy Gid F" first="France" last="Javoy-Agid">France Javoy-Agid</name><affiliation><mods:affiliation>Unité INSERM 289, Paris</mods:affiliation></affiliation></author><author><name sortKey="Hauw, Jean Acques" sort="Hauw, Jean Acques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name><affiliation><mods:affiliation>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><mods:affiliation>Unité INSERM 289, Paris</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:92C19D9A1CC945E3A79C5D9E989ECAD981A32482</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1002/ana.410330506</idno><idno type="url">https://api.istex.fr/document/92C19D9A1CC945E3A79C5D9E989ECAD981A32482/fulltext/pdf</idno><idno 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France</mods:affiliation></affiliation></author><author><name sortKey="Javoy Gid, France" sort="Javoy Gid, France" uniqKey="Javoy Gid F" first="France" last="Javoy-Agid">France Javoy-Agid</name><affiliation><mods:affiliation>Unité INSERM 289, Paris</mods:affiliation></affiliation></author><author><name sortKey="Hauw, Jean Acques" sort="Hauw, Jean Acques" uniqKey="Hauw J" first="Jean-Jacques" last="Hauw">Jean-Jacques Hauw</name><affiliation><mods:affiliation>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name><affiliation><mods:affiliation>Unité INSERM 289, Paris</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="ISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1993-05">1993-05</date><biblScope unit="volume">33</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="445">445</biblScope><biblScope unit="page" to="450">450</biblScope></imprint><idno type="ISSN">0364-5134</idno></series><idno type="istex">92C19D9A1CC945E3A79C5D9E989ECAD981A32482</idno><idno type="DOI">10.1002/ana.410330506</idno><idno type="ArticleID">ANA410330506</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0364-5134</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Patrick Vermersch MD</name><affiliations><json:string>Unité INSERM 156, Lille</json:string></affiliations></json:item><json:item><name>Dr. Delacourte PhD</name><affiliations><json:string>Unité INSERM 156, Lille</json:string><json:string>Unité INSERM 156, Place de Verdun, 59045 Lille cedex, France</json:string></affiliations></json:item><json:item><name>France Javoy‐Agid PhD</name><affiliations><json:string>Unité INSERM 289, Paris</json:string></affiliations></json:item><json:item><name>Jean‐Jacques Hauw MD</name><affiliations><json:string>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</json:string></affiliations></json:item><json:item><name>Yves Agid MD, PhD</name><affiliations><json:string>Unité INSERM 289, Paris</json:string></affiliations></json:item></author><articleId><json:string>ANA410330506</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</abstract><qualityIndicators><score>6.383</score><pdfVersion>1.3</pdfVersion><pdfPageSize>576 x 828 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1451</abstractCharCount><pdfWordCount>3887</pdfWordCount><pdfCharCount>24436</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>208</abstractWordCount></qualityIndicators><title>Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins</title><refBibs><json:item><author><json:item><name>JL Cummings</name></json:item></author><host><volume>28</volume><pages><last>23</last><first>15</first></pages><author></author><title>Eur 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proteins</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Copyright © 1993 The American Neurological Assosiation</p></availability><date>1993</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins</title><author xml:id="author-1"><persName><forename type="first">Patrick</forename><surname>Vermersch</surname></persName><roleName type="degree">MD</roleName><affiliation>Unité INSERM 156, Lille</affiliation></author><author xml:id="author-2"><persName><surname>Delacourte</surname></persName><roleName type="degree">Dr.</roleName><affiliation>Unité INSERM 156, Lille</affiliation><affiliation>Unité INSERM 156, Place de Verdun, 59045 Lille cedex, France</affiliation></author><author xml:id="author-3"><persName><forename type="first">France</forename><surname>Javoy‐Agid</surname></persName><roleName type="degree">PhD</roleName><affiliation>Unité INSERM 289, Paris</affiliation></author><author xml:id="author-4"><persName><forename type="first">Jean‐Jacques</forename><surname>Hauw</surname></persName><roleName type="degree">MD</roleName><affiliation>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</affiliation></author><author xml:id="author-5"><persName><forename type="first">Yves</forename><surname>Agid</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Unité INSERM 289, Paris</affiliation></author></analytic><monogr><title level="j">Annals of Neurology</title><title level="j" type="sub">Official Journal of the American Neurological Association and the Child Neurology Society</title><title level="j" type="abbrev">Ann Neurol.</title><idno type="pISSN">0364-5134</idno><idno type="eISSN">1531-8249</idno><idno type="DOI">10.1002/(ISSN)1531-8249</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1993-05"></date><biblScope unit="volume">33</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="445">445</biblScope><biblScope unit="page" to="450">450</biblScope></imprint></monogr><idno type="istex">92C19D9A1CC945E3A79C5D9E989ECAD981A32482</idno><idno type="DOI">10.1002/ana.410330506</idno><idno type="ArticleID">ANA410330506</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1993</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Original Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1992-08-25">Received</change><change when="1992-12-02">Registration</change><change when="1993-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/92C19D9A1CC945E3A79C5D9E989ECAD981A32482/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" 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proteins</title><title type="short" xml:lang="en">Abnormal Tau Proteins in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Patrick</givenNames><familyName>Vermersch</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>André</givenNames><familyName>Delacourte</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>France</givenNames><familyName>Javoy‐Agid</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jean‐Jacques</givenNames><familyName>Hauw</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Yves</givenNames><familyName>Agid</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FR" type="organization"><unparsedAffiliation>Unité INSERM 156, Lille</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FR" type="organization"><unparsedAffiliation>Unité INSERM 289, Paris</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FR" type="organization"><unparsedAffiliation>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abnormal Tau Proteins in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Dementia in Parkinson's disease: Biochemical evidence for cortical involvement using the immunodetection of abnormal tau proteins</title></titleInfo><name type="personal"><namePart type="given">Patrick</namePart><namePart type="family">Vermersch</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Unité INSERM 156, Lille</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Delacourte</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Unité INSERM 156, Lille</affiliation><affiliation>Unité INSERM 156, Place de Verdun, 59045 Lille cedex, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">France</namePart><namePart type="family">Javoy‐Agid</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Unité INSERM 289, Paris</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jean‐Jacques</namePart><namePart type="family">Hauw</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Laboratoire de Neuropathologie Raymond Escourolle, Hǒpital de La Salpětrière, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yves</namePart><namePart type="family">Agid</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Unité INSERM 289, Paris</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">1993-05</dateIssued><dateCaptured encoding="w3cdtf">1992-08-25</dateCaptured><dateValid encoding="w3cdtf">1992-12-02</dateValid><copyrightDate encoding="w3cdtf">1993</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="references">50</extent></physicalDescription><abstract lang="en">In order to elucidate the neurochemical basis of the dementia of Parkinson's disease, we compared samples of cerebral cortex from 24 nondemented parkinsonian patients and parkinsonian patients with various degrees of dementia, with those from patients with Alzheimer's disease and control subjects, using a quantitative Western blot analysis. An anti‐paired helical filaments antibody was used for the immunodetection of the abnormally phosphorylated Tau proteins 55,64, and 69, which are known to be specific and reliable biochemical markers of Alzaheimer‐type neurofibrillary degeneration. The frequency and intensity of immunodetection of the abnormal Tau triplet were higher in the demented parkinsonian subgroups than in the nondemented parkinsonian subgroup in the prefrontal area, temporal cortex, and entorhinal cortex but not in either the occipital or the cingular cortex. A quantification of abnormal Tau triplet by densaitometry showed that unlike the results obtained in Alzheimer patients, the intensity of lesions in the cerebral cortex of the most demented parkinsonian patients was more severe in the prefrontal area versus the temporal area. This study (1) gives biochemical evidence for Alzheimer‐type changes in the cortex of demented parkinsonian patients and (2) suggests that lesions of the prefrontal cortex may significantly contribute to the occurrence of cognitive changes at least in some patients with Parkinson's disease.</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>Original 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>1993</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>445</start><end>450</end><total>6</total></extent></part></relatedItem><identifier type="istex">92C19D9A1CC945E3A79C5D9E989ECAD981A32482</identifier><identifier type="DOI">10.1002/ana.410330506</identifier><identifier type="ArticleID">ANA410330506</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1993 The American Neurological Assosiation</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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