Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins
Identifieur interne : 001506 ( Istex/Corpus ); précédent : 001505; suivant : 001507Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins
Auteurs : Claudia Schwab ; John C. Steele ; Patrick L. McgeerSource :
- Brain Research [ 0006-8993 ] ; 1996.
English descriptors
- KwdEn :
Abstract
Guamanian parkinsonism-dementia, locally described as bodig, is characterized by the widespread appearance of neurofibrillary tangles in cortical and subcortical areas. These tangles have similar regional distribution and immunohistochemical profile to those found in Alzheimer disease (AD). We studied the immunohistochemical staining of these tangles, as well as those of AD, using antibodies to complement proteins and related molecules. In bodig, as in AD, extracellular tangles were intensely decorated with antibodies to C1q, C4d and C3d, but not fraction Bb of factor B, properidin or immunoglobulins. This is evidence that the classical, but not the alternative complement pathway is activated on extracellular tangles and that the activation is independent of antibodies. Immunohistochemical staining for amyloid P, an in vitro activator of complement, was remarkably similar to that for the Clq, C4d and Cad in both bodig and AD. This was not the case for ß-amyloid protein (BAP), another in vitro complement activator. Positive staining was observed in only a minority of extracellular tangles in bodig and was only rarely observed in those of AD. BAP would therefore not appear to be a candidate for activating complement on extracellular neurofibrillary tangles. Reactive microglia and reactive astrocytes were closely associated with complement positive extracellular neurofibrillary tangles, indicating an inflammatory response similar to that seen in AD.
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DOI: 10.1016/0006-8993(95)01257-5
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Mcgeer</name><affiliation><mods:affiliation>Corresponding author. Fax: (1) (604) 822-7086.</mods:affiliation></affiliation><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0A098236B887108FDF69547B040B01E710E23399</idno><date when="1996" year="1996">1996</date><idno type="doi">10.1016/0006-8993(95)01257-5</idno><idno type="url">https://api-v5.istex.fr/document/0A098236B887108FDF69547B040B01E710E23399/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001506</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001506</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins</title><author><name sortKey="Schwab, Claudia" sort="Schwab, Claudia" uniqKey="Schwab C" first="Claudia" last="Schwab">Claudia Schwab</name><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</mods:affiliation></affiliation></author><author><name sortKey="Steele, John C" sort="Steele, John C" uniqKey="Steele J" first="John C." last="Steele">John C. Steele</name><affiliation><mods:affiliation>Guam Memorial Hospital, Agana, Guam</mods:affiliation></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation><mods:affiliation>Corresponding author. Fax: (1) (604) 822-7086.</mods:affiliation></affiliation><affiliation><mods:affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="ISSN">0006-8993</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996">1996</date><biblScope unit="volume">707</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="196">196</biblScope><biblScope unit="page" to="205">205</biblScope></imprint><idno type="ISSN">0006-8993</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8993</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term><term>Amyloid P</term><term>Inflammation</term><term>Microglia</term><term>Reactive astrocyte</term><term>β-Amyloid protein</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Guamanian parkinsonism-dementia, locally described as bodig, is characterized by the widespread appearance of neurofibrillary tangles in cortical and subcortical areas. These tangles have similar regional distribution and immunohistochemical profile to those found in Alzheimer disease (AD). We studied the immunohistochemical staining of these tangles, as well as those of AD, using antibodies to complement proteins and related molecules. In bodig, as in AD, extracellular tangles were intensely decorated with antibodies to C1q, C4d and C3d, but not fraction Bb of factor B, properidin or immunoglobulins. This is evidence that the classical, but not the alternative complement pathway is activated on extracellular tangles and that the activation is independent of antibodies. Immunohistochemical staining for amyloid P, an in vitro activator of complement, was remarkably similar to that for the Clq, C4d and Cad in both bodig and AD. This was not the case for ß-amyloid protein (BAP), another in vitro complement activator. Positive staining was observed in only a minority of extracellular tangles in bodig and was only rarely observed in those of AD. BAP would therefore not appear to be a candidate for activating complement on extracellular neurofibrillary tangles. Reactive microglia and reactive astrocytes were closely associated with complement positive extracellular neurofibrillary tangles, indicating an inflammatory response similar to that seen in AD.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Claudia Schwab</name><affiliations><json:string>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</json:string></affiliations></json:item><json:item><name>John C. Steele</name><affiliations><json:string>Guam Memorial Hospital, Agana, Guam</json:string></affiliations></json:item><json:item><name>Patrick L. McGeer</name><affiliations><json:string>Corresponding author. 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Fax: (1) (604) 822-7086.</affiliation><affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</affiliation></author><idno type="istex">0A098236B887108FDF69547B040B01E710E23399</idno><idno type="DOI">10.1016/0006-8993(95)01257-5</idno><idno type="PII">0006-8993(95)01257-5</idno><idno type="ArticleID">95012575</idno></analytic><monogr><title level="j">Brain Research</title><title level="j" type="abbrev">BRES</title><idno type="pISSN">0006-8993</idno><idno type="PII">S0006-8993(00)X0020-0</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1996"></date><biblScope unit="volume">707</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="196">196</biblScope><biblScope unit="page" to="205">205</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1996</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Guamanian parkinsonism-dementia, locally described as bodig, is characterized by the widespread appearance of neurofibrillary tangles in cortical and subcortical areas. These tangles have similar regional distribution and immunohistochemical profile to those found in Alzheimer disease (AD). We studied the immunohistochemical staining of these tangles, as well as those of AD, using antibodies to complement proteins and related molecules. In bodig, as in AD, extracellular tangles were intensely decorated with antibodies to C1q, C4d and C3d, but not fraction Bb of factor B, properidin or immunoglobulins. This is evidence that the classical, but not the alternative complement pathway is activated on extracellular tangles and that the activation is independent of antibodies. Immunohistochemical staining for amyloid P, an in vitro activator of complement, was remarkably similar to that for the Clq, C4d and Cad in both bodig and AD. This was not the case for ß-amyloid protein (BAP), another in vitro complement activator. Positive staining was observed in only a minority of extracellular tangles in bodig and was only rarely observed in those of AD. BAP would therefore not appear to be a candidate for activating complement on extracellular neurofibrillary tangles. Reactive microglia and reactive astrocytes were closely associated with complement positive extracellular neurofibrillary tangles, indicating an inflammatory response similar to that seen in AD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Alzheimer disease</term></item><item><term>Amyloid P</term></item><item><term>β-Amyloid protein</term></item><item><term>Reactive astrocyte</term></item><item><term>Microglia</term></item><item><term>Inflammation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/0A098236B887108FDF69547B040B01E710E23399/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>BRES</jid><aid>95012575</aid><ce:pii>0006-8993(95)01257-5</ce:pii><ce:doi>10.1016/0006-8993(95)01257-5</ce:doi><ce:copyright type="unknown" year="1996"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Research report</ce:textfn></ce:dochead><ce:title>Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins</ce:title><ce:author-group><ce:author><ce:given-name>Claudia</ce:given-name><ce:surname>Schwab</ce:surname><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>John C.</ce:given-name><ce:surname>Steele</ce:surname><ce:cross-ref refid="AFF2"><ce:sup loc="post">b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Patrick L.</ce:given-name><ce:surname>McGeer</ce:surname><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref><ce:cross-ref refid="AFF1"><ce:sup loc="post">a</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Guam Memorial Hospital, Agana, Guam</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Corresponding author. Fax: (1) (604) 822-7086.</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="28" month="9" year="1995"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Guamanian parkinsonism-dementia, locally described as bodig, is characterized by the widespread appearance of neurofibrillary tangles in cortical and subcortical areas. These tangles have similar regional distribution and immunohistochemical profile to those found in Alzheimer disease (AD). We studied the immunohistochemical staining of these tangles, as well as those of AD, using antibodies to complement proteins and related molecules. In bodig, as in AD, extracellular tangles were intensely decorated with antibodies to C1q, C4d and C3d, but not fraction Bb of factor B, properidin or immunoglobulins. This is evidence that the classical, but not the alternative complement pathway is activated on extracellular tangles and that the activation is independent of antibodies. Immunohistochemical staining for amyloid P, an in vitro activator of complement, was remarkably similar to that for the Clq, C4d and Cad in both bodig and AD. This was not the case for ß-amyloid protein (BAP), another in vitro complement activator. Positive staining was observed in only a minority of extracellular tangles in bodig and was only rarely observed in those of AD. BAP would therefore not appear to be a candidate for activating complement on extracellular neurofibrillary tangles. Reactive microglia and reactive astrocytes were closely associated with complement positive extracellular neurofibrillary tangles, indicating an inflammatory response similar to that seen in AD.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Alzheimer disease</ce:text></ce:keyword><ce:keyword><ce:text>Amyloid P</ce:text></ce:keyword><ce:keyword><ce:text>β-Amyloid protein</ce:text></ce:keyword><ce:keyword><ce:text>Reactive astrocyte</ce:text></ce:keyword><ce:keyword><ce:text>Microglia</ce:text></ce:keyword><ce:keyword><ce:text>Inflammation</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins</title></titleInfo><name type="personal"><namePart type="given">Claudia</namePart><namePart type="family">Schwab</namePart><affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John C.</namePart><namePart type="family">Steele</namePart><affiliation>Guam Memorial Hospital, Agana, Guam</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Patrick L.</namePart><namePart type="family">McGeer</namePart><affiliation>Corresponding author. Fax: (1) (604) 822-7086.</affiliation><affiliation>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1996</dateIssued><copyrightDate encoding="w3cdtf">1996</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Guamanian parkinsonism-dementia, locally described as bodig, is characterized by the widespread appearance of neurofibrillary tangles in cortical and subcortical areas. These tangles have similar regional distribution and immunohistochemical profile to those found in Alzheimer disease (AD). We studied the immunohistochemical staining of these tangles, as well as those of AD, using antibodies to complement proteins and related molecules. In bodig, as in AD, extracellular tangles were intensely decorated with antibodies to C1q, C4d and C3d, but not fraction Bb of factor B, properidin or immunoglobulins. This is evidence that the classical, but not the alternative complement pathway is activated on extracellular tangles and that the activation is independent of antibodies. Immunohistochemical staining for amyloid P, an in vitro activator of complement, was remarkably similar to that for the Clq, C4d and Cad in both bodig and AD. This was not the case for ß-amyloid protein (BAP), another in vitro complement activator. Positive staining was observed in only a minority of extracellular tangles in bodig and was only rarely observed in those of AD. BAP would therefore not appear to be a candidate for activating complement on extracellular neurofibrillary tangles. Reactive microglia and reactive astrocytes were closely associated with complement positive extracellular neurofibrillary tangles, indicating an inflammatory response similar to that seen in AD.</abstract><note type="content">Section title: Research report</note><subject lang="en"><genre>Keywords</genre><topic>Alzheimer disease</topic><topic>Amyloid P</topic><topic>β-Amyloid protein</topic><topic>Reactive astrocyte</topic><topic>Microglia</topic><topic>Inflammation</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research</title></titleInfo><titleInfo type="abbreviated"><title>BRES</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">19960129</dateIssued></originInfo><identifier type="ISSN">0006-8993</identifier><identifier type="PII">S0006-8993(00)X0020-0</identifier><part><date>19960129</date><detail type="volume"><number>707</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue pages"><start>139</start><end>328</end></extent><extent unit="pages"><start>196</start><end>205</end></extent></part></relatedItem><identifier type="istex">0A098236B887108FDF69547B040B01E710E23399</identifier><identifier type="DOI">10.1016/0006-8993(95)01257-5</identifier><identifier type="PII">0006-8993(95)01257-5</identifier><identifier type="ArticleID">95012575</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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