Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex
Identifieur interne : 000551 ( Main/Corpus ); précédent : 000550; suivant : 000552Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex
Auteurs : H. Braak ; E. BraakSource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1990-03-01.
Abstract
Summary: Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.
Url:
DOI: 10.1007/BF02251245
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Braak</name><affiliation><mods:affiliation>Zentrum der Morphologie, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main 70, Federal Republic of Germany</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:CBA8AB4A8F8BFD97C8C3C64C3B1428A0D2885D1E</idno><date when="1990" year="1990">1990</date><idno type="doi">10.1007/BF02251245</idno><idno type="url">https://api.istex.fr/document/CBA8AB4A8F8BFD97C8C3C64C3B1428A0D2885D1E/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000551</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex</title><author><name sortKey="Braak, H" sort="Braak, H" uniqKey="Braak H" first="H." last="Braak">H. 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In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>Dr. H. Braak</name><affiliations><json:string>Zentrum der Morphologie, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main 70, Federal Republic of Germany</json:string></affiliations></json:item><json:item><name>E. Braak</name><affiliations><json:string>Zentrum der Morphologie, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main 70, Federal Republic of Germany</json:string></affiliations></json:item></author><articleId><json:string>Art6</json:string><json:string>BF02251245</json:string></articleId><language><json:string>eng</json:string></language><abstract>Summary: Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. 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In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989-07-18">Created</change><change when="1990-03-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/CBA8AB4A8F8BFD97C8C3C64C3B1428A0D2885D1E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>722</JournalID><JournalPrintISSN>0936-3076</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</JournalTitle><JournalAbbreviatedTitle>J Neural Transm Gen Sect</JournalAbbreviatedTitle><JournalSubjectGroup><JournalSubject Type="Primary">Medicine & Public Health</JournalSubject><JournalSubject Type="Secondary">Pharmacology/Toxicology</JournalSubject><JournalSubject Type="Secondary">Psychiatry</JournalSubject><JournalSubject Type="Secondary">Neurology</JournalSubject></JournalSubjectGroup></JournalInfo><Volume><VolumeInfo VolumeType="Regular" TocLevels="0"><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><VolumeIssueCount>4</VolumeIssueCount></VolumeInfo><Issue IssueType="Regular"><IssueInfo TocLevels="0"><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd><IssueArticleCount>8</IssueArticleCount><IssueHistory><CoverDate><DateString>1990</DateString><Year>1990</Year><Month>3</Month></CoverDate></IssueHistory><IssueCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</CopyrightYear></IssueCopyright></IssueInfo><Article ID="Art6"><ArticleInfo Language="En" ArticleType="OriginalPaper" NumberingStyle="Unnumbered" TocLevels="0" ContainsESM="No"><ArticleID>BF02251245</ArticleID><ArticleDOI>10.1007/BF02251245</ArticleDOI><ArticleSequenceNumber>6</ArticleSequenceNumber><ArticleTitle Language="En">Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex</ArticleTitle><ArticleCategory>Original Papers</ArticleCategory><ArticleFirstPage>45</ArticleFirstPage><ArticleLastPage>57</ArticleLastPage><ArticleHistory><RegistrationDate><Year>2005</Year><Month>10</Month><Day>24</Day></RegistrationDate><Received><Year>1989</Year><Month>7</Month><Day>18</Day></Received><Accepted><Year>1989</Year><Month>9</Month><Day>26</Day></Accepted></ArticleHistory><ArticleCopyright><CopyrightHolderName>Springer-Verlag</CopyrightHolderName><CopyrightYear>1990</CopyrightYear></ArticleCopyright><ArticleGrants Type="Regular"><MetadataGrant Grant="OpenAccess"></MetadataGrant><AbstractGrant Grant="OpenAccess"></AbstractGrant><BodyPDFGrant Grant="Restricted"></BodyPDFGrant><BodyHTMLGrant Grant="Restricted"></BodyHTMLGrant><BibliographyGrant Grant="Restricted"></BibliographyGrant><ESMGrant Grant="Restricted"></ESMGrant></ArticleGrants><ArticleContext><JournalID>722</JournalID><VolumeIDStart>2</VolumeIDStart><VolumeIDEnd>2</VolumeIDEnd><IssueIDStart>1</IssueIDStart><IssueIDEnd>1</IssueIDEnd></ArticleContext></ArticleInfo><ArticleHeader><AuthorGroup><Author AffiliationIDS="Aff1" PresentAffiliationID="Aff1"><AuthorName DisplayOrder="Western"><Prefix>Dr.</Prefix><GivenName>H.</GivenName><FamilyName>Braak</FamilyName></AuthorName></Author><Author AffiliationIDS="Aff1"><AuthorName DisplayOrder="Western"><GivenName>E.</GivenName><FamilyName>Braak</FamilyName></AuthorName></Author><Affiliation ID="Aff1"><OrgName>Zentrum der Morphologie</OrgName><OrgAddress><Street>Theodor-Stern-Kai 7</Street><Postcode>D-6000</Postcode><City>Frankfurt/Main 70</City><Country>Federal Republic of Germany</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Parkinson's disease</Keyword><Keyword>cognitive impairment</Keyword><Keyword>amyloid</Keyword><Keyword>neurofibrillary tangles</Keyword><Keyword>neuropil threads</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="given">H.</namePart><namePart type="family">Braak</namePart><affiliation>Zentrum der Morphologie, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Braak</namePart><affiliation>Zentrum der Morphologie, Theodor-Stern-Kai 7, D-6000, Frankfurt/Main 70, Federal Republic of Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="OriginalPaper"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1989-07-18</dateCreated><dateIssued encoding="w3cdtf">1990-03-01</dateIssued><copyrightDate encoding="w3cdtf">1990</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-α of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. 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