Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins
Identifieur interne : 003E25 ( Main/Exploration ); précédent : 003E24; suivant : 003E26Neurofibrillary tangles of Guam parkinson-dementia are associated with reactive microglia and complement proteins
Auteurs : Claudia Schwab [Canada] ; John C. Steele ; Patrick L. Mcgeer [Canada]Source :
- Brain Research [ 0006-8993 ] ; 1996.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Alzheimer disease, Amyloid P, Amyloid beta-Peptides (metabolism), Amyotrophic Lateral Sclerosis (pathology), Astrocyte, Astrocytes (physiology), Brain (pathology), Classical pathway complement, Complement Pathway, Classical, Complement System Proteins (metabolism), Dementia (pathology), Female, Guam, Guam Parkinson dementia, Histopathology, Human, Humans, Immunohistochemistry, Inflammation, Male, Microglia, Microglia (physiology), Middle Aged, Neurofibrillary Tangles (pathology), Neurofibrillary tangle, Parkinson Disease (pathology), Reactive astrocyte, Syndrome, β Amyloid protein, β-Amyloid protein.
- MESH :
- chemical , metabolism : Amyloid beta-Peptides, Complement System Proteins.
- geographic : Guam.
- pathology : Amyotrophic Lateral Sclerosis, Brain, Dementia, Neurofibrillary Tangles, Parkinson Disease.
- physiology : Astrocytes, Microglia.
- Adult, Aged, Aged, 80 and over, Complement Pathway, Classical, Female, Humans, Immunohistochemistry, Male, Middle Aged, Syndrome.
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.
Url:
DOI: 10.1016/0006-8993(95)01257-5
Affiliations:
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Le document en format XML
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Steele</name><affiliation><wicri:noCountry code="subField">Guam</wicri:noCountry></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></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC V6T 1Z3</wicri:regionArea><wicri:noRegion>BC V6T 1Z3</wicri:noRegion></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>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Alzheimer disease</term><term>Amyloid P</term><term>Amyloid beta-Peptides (metabolism)</term><term>Amyotrophic Lateral Sclerosis (pathology)</term><term>Astrocyte</term><term>Astrocytes (physiology)</term><term>Brain (pathology)</term><term>Classical pathway complement</term><term>Complement Pathway, Classical</term><term>Complement System Proteins (metabolism)</term><term>Dementia (pathology)</term><term>Female</term><term>Guam</term><term>Guam Parkinson dementia</term><term>Histopathology</term><term>Human</term><term>Humans</term><term>Immunohistochemistry</term><term>Inflammation</term><term>Male</term><term>Microglia</term><term>Microglia (physiology)</term><term>Middle Aged</term><term>Neurofibrillary Tangles (pathology)</term><term>Neurofibrillary tangle</term><term>Parkinson Disease (pathology)</term><term>Reactive astrocyte</term><term>Syndrome</term><term>β Amyloid protein</term><term>β-Amyloid protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Complement System Proteins</term></keywords><keywords scheme="MESH" type="geographic" xml:lang="en"><term>Guam</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Amyotrophic Lateral Sclerosis</term><term>Brain</term><term>Dementia</term><term>Neurofibrillary Tangles</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Astrocytes</term><term>Microglia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Complement Pathway, Classical</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Middle Aged</term><term>Syndrome</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Amyloïde P</term><term>Astrocyte</term><term>Complément voie classique</term><term>Histopathologie</term><term>Homme</term><term>Inflammation</term><term>Microglie</term><term>Parkinson démence ile de Guam</term><term>Protéine amyloïde β</term><term>Structure neurofibrillaire</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</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><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Steele, John C" sort="Steele, John C" uniqKey="Steele J" first="John C." last="Steele">John C. Steele</name></noCountry><country name="Canada"><noRegion><name sortKey="Schwab, Claudia" sort="Schwab, Claudia" uniqKey="Schwab C" first="Claudia" last="Schwab">Claudia Schwab</name></noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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