Apolipoprotein E4 (ApoE4) but not ApoE3 or ApoE2 potentiates β-amyloid protein activation of complement in vitro
Identifieur interne : 003C10 ( Main/Exploration ); précédent : 003C09; suivant : 003C11Apolipoprotein E4 (ApoE4) but not ApoE3 or ApoE2 potentiates β-amyloid protein activation of complement in vitro
Auteurs : Patrick L. Mcgeer [Canada] ; Douglas G. Walker [Canada] ; Robert E. Pitas [États-Unis] ; Robert W. Mahley [États-Unis] ; Edith G. Mcgeer [Canada]Source :
- Brain Research [ 0006-8993 ] ; 1997.
English descriptors
- KwdEn :
Abstract
Apolipoprotein E4 (ApoE4) increases the risk of late-onset Alzheimer's disease (AD). It binds tightly to β-amyloid protein (A β), which is known to activate the classical complement pathway in vitro. Since complement activation is a possible mechanism for promoting inflammation in AD, we tested, utilizing ELISA techniques, whether the various isoforms of ApoE could influence A β complement activation, or could themselves activate the pathway. A β applied alone to ELISA plate wells at concentrations of 100–500 ng showed a linear increase in ability to activate serum complement, but all the ApoE isoproteins were inactive. When 200 or 430 ng of A β were plated and then exposed to solutions of 100–200 ng of ApoE2, ApoE3, ApoE4 or bovine serum albumin (BSA), only ApoE4 significantly enhanced the activation. This ApoE4-specific enhancement of complement activation by A β may relate to its role in increasing the risk of late-onset AD.
Url:
DOI: 10.1016/S0006-8993(96)01324-8
Affiliations:
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Pitas</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Gladstone Institute of Cardiovascular Disease, Cardiovascular Research Institute and Department of Pathology, University of California at San Francisco, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Mahley, Robert W" sort="Mahley, Robert W" uniqKey="Mahley R" first="Robert W." last="Mahley">Robert W. 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Mcgeer</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, BC</wicri:regionArea><wicri:noRegion>BC</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="1997">1997</date><biblScope unit="volume">749</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="138">138</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's disease</term><term>Binding</term><term>Inflammation</term><term>Senile plaque</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Apolipoprotein E4 (ApoE4) increases the risk of late-onset Alzheimer's disease (AD). It binds tightly to β-amyloid protein (A β), which is known to activate the classical complement pathway in vitro. Since complement activation is a possible mechanism for promoting inflammation in AD, we tested, utilizing ELISA techniques, whether the various isoforms of ApoE could influence A β complement activation, or could themselves activate the pathway. A β applied alone to ELISA plate wells at concentrations of 100–500 ng showed a linear increase in ability to activate serum complement, but all the ApoE isoproteins were inactive. When 200 or 430 ng of A β were plated and then exposed to solutions of 100–200 ng of ApoE2, ApoE3, ApoE4 or bovine serum albumin (BSA), only ApoE4 significantly enhanced the activation. This ApoE4-specific enhancement of complement activation by A β may relate to its role in increasing the risk of late-onset AD.</div></front></TEI><affiliations><list><country><li>Canada</li><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name></noRegion><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Pitas, Robert E" sort="Pitas, Robert E" uniqKey="Pitas R" first="Robert E." last="Pitas">Robert E. Pitas</name></region><name sortKey="Mahley, Robert W" sort="Mahley, Robert W" uniqKey="Mahley R" first="Robert W." last="Mahley">Robert W. Mahley</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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