Distinct distribution of apolipoprotein E and β-amyloid immunoreactivity in the hippocampus of Parkinson dementia complex of Guam
Identifieur interne : 004598 ( Main/Merge ); précédent : 004597; suivant : 004599Distinct distribution of apolipoprotein E and β-amyloid immunoreactivity in the hippocampus of Parkinson dementia complex of Guam
Auteurs : C. Schwab [Canada] ; J. C. Steele ; H. Akiyama [Japon] ; P. L. Mcgeer [Canada]Source :
- Acta neuropathologica [ 0001-6322 ] ; 1996.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
Abstract
The distribution of apolipoprotein E (ApoE) was studied in the brain tissue of cases of the amyotrophic lateral sclerosis - parkinsonism - dementia complex of Guam, locally known as lytico bodig disease (LB), and compared with cases of Alzheimer's disease (AD) and normal brain tissue. In both LB and AD, strong ApoE immunostaining was observed in association with pathological lesions. In LB, these were mainly extracellular neurofibrillary tangles (eNFTs) which were intensely immunopositive for ApoE. Occasional diffuse β-amyloid protein (βAP) deposits appear in this disorder and they were moderately immunopositive. In AD, senile plaques and diffuse βAP deposits were intensely immunopositive, while eNFTs were only moderately immunopositive. The reason for the strong association of ApoE with the pathological entities in LB and AD is unknown, but may be related to a scavenger function which does not involve lipid metabolism. In both LB and AD, subpial and layer I diffuse deposits were ApoE negative but βAP positive. Intracellular NFTs were mostly ApoE negative. A few showed weak positive staining. These data suggest that ApoE appears in LB and AD pathological lesions only after they are well established. In all controls, as well as all LB and AD cases, strong ApoE immunoreactivity was observed in unidentifiable structures in capillaries. Weak staining in a few neurons and very weak staining of an occasional astrocyte was observed. The source of ApoE which is deposited on extracellular pathological structures in LB and AD is unknown.
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Steele</name><affiliation><inist:fA14 i1="02"><s1>Guam Memorial Hospital</s1><s2>Agana</s2><s3>GUM</s3><sZ>2 aut.</sZ></inist:fA14><wicri:noCountry>GUM</wicri:noCountry></affiliation></author><author><name sortKey="Akiyama, H" sort="Akiyama, H" uniqKey="Akiyama H" first="H." last="Akiyama">H. Akiyama</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Tokyo Institute of Psychiatry, 2-1-8, Kamikitazawa</s1><s2>Setagaya-ku, Tokyo 156</s2><s3>JPN</s3><sZ>3 aut.</sZ></inist:fA14><country>Japon</country><placeName><settlement type="city">Tokyo</settlement></placeName></affiliation></author><author><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P. L." last="Mcgeer">P. L. Mcgeer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall</s1><s2>Vancouver, B.C., V6T 1Z3</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, B.C., V6T 1Z3</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">96-0432307</idno><date when="1996">1996</date><idno type="stanalyst">PASCAL 96-0432307 INIST</idno><idno type="RBID">Pascal:96-0432307</idno><idno type="wicri:Area/PascalFrancis/Corpus">000F25</idno><idno type="wicri:Area/PascalFrancis/Curation">000F98</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000E32</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000E32</idno><idno type="wicri:doubleKey">0001-6322:1996:Schwab C:distinct:distribution:of</idno><idno type="wicri:Area/Main/Merge">004598</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Distinct distribution of apolipoprotein E and β-amyloid immunoreactivity in the hippocampus of Parkinson dementia complex of Guam</title><author><name sortKey="Schwab, C" sort="Schwab, C" uniqKey="Schwab C" first="C." last="Schwab">C. Schwab</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall</s1><s2>Vancouver, B.C., V6T 1Z3</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, B.C., V6T 1Z3</wicri:noRegion></affiliation></author><author><name sortKey="Steele, J C" sort="Steele, J C" uniqKey="Steele J" first="J. C." last="Steele">J. C. Steele</name><affiliation><inist:fA14 i1="02"><s1>Guam Memorial Hospital</s1><s2>Agana</s2><s3>GUM</s3><sZ>2 aut.</sZ></inist:fA14><wicri:noCountry>GUM</wicri:noCountry></affiliation></author><author><name sortKey="Akiyama, H" sort="Akiyama, H" uniqKey="Akiyama H" first="H." last="Akiyama">H. Akiyama</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Tokyo Institute of Psychiatry, 2-1-8, Kamikitazawa</s1><s2>Setagaya-ku, Tokyo 156</s2><s3>JPN</s3><sZ>3 aut.</sZ></inist:fA14><country>Japon</country><placeName><settlement type="city">Tokyo</settlement></placeName></affiliation></author><author><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P. L." last="Mcgeer">P. L. Mcgeer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Kinsmen Laboratory of Neurological Research and the Neurodegenerative Disorders Centre, University of British Columbia, 2255 Wesbrook Mall</s1><s2>Vancouver, B.C., V6T 1Z3</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, B.C., V6T 1Z3</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Acta neuropathologica</title><title level="j" type="abbreviated">Acta neuropathol.</title><idno type="ISSN">0001-6322</idno><imprint><date when="1996">1996</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Acta neuropathologica</title><title level="j" type="abbreviated">Acta neuropathol.</title><idno type="ISSN">0001-6322</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alzheimer disease</term><term>Amyloid</term><term>Apolipoprotein E</term><term>Comparative study</term><term>Guam Parkinson dementia</term><term>Hippocampus</term><term>Human</term><term>Immunoblotting assay</term><term>Immunohistochemistry</term><term>Neurofibrillary tangle</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Parkinson démence ile de Guam</term><term>Démence Alzheimer</term><term>Immunohistochimie</term><term>Hippocampe</term><term>Méthode immunoblotting</term><term>Apolipoprotéine E</term><term>Amyloïde</term><term>Structure neurofibrillaire</term><term>Etude comparative</term><term>Homme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The distribution of apolipoprotein E (ApoE) was studied in the brain tissue of cases of the amyotrophic lateral sclerosis - parkinsonism - dementia complex of Guam, locally known as lytico bodig disease (LB), and compared with cases of Alzheimer's disease (AD) and normal brain tissue. In both LB and AD, strong ApoE immunostaining was observed in association with pathological lesions. In LB, these were mainly extracellular neurofibrillary tangles (eNFTs) which were intensely immunopositive for ApoE. Occasional diffuse β-amyloid protein (βAP) deposits appear in this disorder and they were moderately immunopositive. In AD, senile plaques and diffuse βAP deposits were intensely immunopositive, while eNFTs were only moderately immunopositive. The reason for the strong association of ApoE with the pathological entities in LB and AD is unknown, but may be related to a scavenger function which does not involve lipid metabolism. In both LB and AD, subpial and layer I diffuse deposits were ApoE negative but βAP positive. Intracellular NFTs were mostly ApoE negative. A few showed weak positive staining. These data suggest that ApoE appears in LB and AD pathological lesions only after they are well established. In all controls, as well as all LB and AD cases, strong ApoE immunoreactivity was observed in unidentifiable structures in capillaries. Weak staining in a few neurons and very weak staining of an occasional astrocyte was observed. The source of ApoE which is deposited on extracellular pathological structures in LB and AD is unknown.</div></front></TEI><affiliations><list><country><li>Canada</li><li>Japon</li></country><settlement><li>Tokyo</li></settlement></list><tree><noCountry><name sortKey="Steele, J C" sort="Steele, J C" uniqKey="Steele J" first="J. C." last="Steele">J. C. Steele</name></noCountry><country name="Canada"><noRegion><name sortKey="Schwab, C" sort="Schwab, C" uniqKey="Schwab C" first="C." last="Schwab">C. Schwab</name></noRegion><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P. L." last="Mcgeer">P. L. Mcgeer</name></country><country name="Japon"><noRegion><name sortKey="Akiyama, H" sort="Akiyama, H" uniqKey="Akiyama H" first="H." last="Akiyama">H. Akiyama</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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