Alzheimer's disease: paired helical filament immunoreactivity in cerebrospinal fluid
Identifieur interne : 002723 ( Main/Exploration ); précédent : 002722; suivant : 002724Alzheimer's disease: paired helical filament immunoreactivity in cerebrospinal fluid
Auteurs : P. Wang [États-Unis] ; K. Iqbal [États-Unis] ; G. Bucht [Suède] ; B. Winblad [Suède] ; M. Wisniewski [États-Unis] ; I. Grundke-Iqbal [États-Unis]Source :
- Acta Neuropathologica [ 0001-6322 ] ; 1991-06-01.
Abstract
Summary: A competitive enzyme-linked immunosorbent assay with high sensitivity has been developed for measuring ubiquitin reactivity of paired helical filaments (PHF). Using the assay, ubiquitin immunoreactivity was estimated in the cerebrospinal fluid (CSF) of 44 patients who had been clinically diagnosed as having Alzheimer's disease (AD) and of 38 control patients, including 20 neurological cases. Monoclonal antibody (mAb) 5–25 to isolated paired helical filaments was used. This mAb recognizes amino acids 64–76 of ubiquitin. The levels of ubiquitin immunoreactivity measured in CSF (twice diluted) were significantly higher in the AD (p<0.001) than in the control group. In only a minority of instances were values for ubiquitin levels the same in AD and control groups: on PHF-coated plates, immunoreactivity values for 77% of the AD CSF specimens were higher than those for 92% of the controls, and on ubiquitin-coated plates, values for 85% of the AD CSF specimens were higher than those for 88% of the controls. On immunoblots of both AD and control CSF, mAb 5-25 stained a series of protein bands. The free ubiquitin that is also present in the CSF was not labeled. No striking differences were detected in the immunoblot pattern of AD and control CSF. This study demonstrastes the presence of quantitative differences in the conjugated ubiquitin in AD and control CSF.
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DOI: 10.1007/BF00310917
Affiliations:
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Wang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Iqbal, K" sort="Iqbal, K" uniqKey="Iqbal K" first="K." last="Iqbal">K. Iqbal</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Bucht, G" sort="Bucht, G" uniqKey="Bucht G" first="G." last="Bucht">G. Bucht</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Geriatric Medicine, University of Umea</wicri:regionArea><wicri:noRegion>University of Umea</wicri:noRegion></affiliation></author><author><name sortKey="Winblad, B" sort="Winblad, B" uniqKey="Winblad B" first="B." last="Winblad">B. Winblad</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Geriatric Medicine, Karolinska Institute, Huddinge Hospital</wicri:regionArea><wicri:noRegion>Huddinge Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Wisniewski, M" sort="Wisniewski, M" uniqKey="Wisniewski M" first="M." last="Wisniewski">M. Wisniewski</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Grundke Iqbal, I" sort="Grundke Iqbal, I" uniqKey="Grundke Iqbal I" first="I." last="Grundke-Iqbal">I. Grundke-Iqbal</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>New York State Institute for Basic Research in Developmental Disabilities, 1050 Forest Hill Road, 10314, Staten Island, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neuropathologica</title><title level="j" type="abbrev">Acta Neuropathol</title><idno type="ISSN">0001-6322</idno><idno type="eISSN">1432-0533</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Berlin/Heidelberg</pubPlace><date type="published" when="1991-06-01">1991-06-01</date><biblScope unit="volume">82</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="6">6</biblScope><biblScope unit="page" to="12">12</biblScope></imprint><idno type="ISSN">0001-6322</idno></series><idno type="istex">3C224E253741F01C4528A5F504673E18A6635272</idno><idno type="DOI">10.1007/BF00310917</idno><idno type="ArticleID">Art2</idno><idno type="ArticleID">BF00310917</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6322</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: A competitive enzyme-linked immunosorbent assay with high sensitivity has been developed for measuring ubiquitin reactivity of paired helical filaments (PHF). Using the assay, ubiquitin immunoreactivity was estimated in the cerebrospinal fluid (CSF) of 44 patients who had been clinically diagnosed as having Alzheimer's disease (AD) and of 38 control patients, including 20 neurological cases. Monoclonal antibody (mAb) 5–25 to isolated paired helical filaments was used. This mAb recognizes amino acids 64–76 of ubiquitin. The levels of ubiquitin immunoreactivity measured in CSF (twice diluted) were significantly higher in the AD (p<0.001) than in the control group. In only a minority of instances were values for ubiquitin levels the same in AD and control groups: on PHF-coated plates, immunoreactivity values for 77% of the AD CSF specimens were higher than those for 92% of the controls, and on ubiquitin-coated plates, values for 85% of the AD CSF specimens were higher than those for 88% of the controls. On immunoblots of both AD and control CSF, mAb 5-25 stained a series of protein bands. The free ubiquitin that is also present in the CSF was not labeled. No striking differences were detected in the immunoblot pattern of AD and control CSF. This study demonstrastes the presence of quantitative differences in the conjugated ubiquitin in AD and control CSF.</div></front></TEI><affiliations><list><country><li>Suède</li><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Wang, P" sort="Wang, P" uniqKey="Wang P" first="P." last="Wang">P. Wang</name></region><name sortKey="Grundke Iqbal, I" sort="Grundke Iqbal, I" uniqKey="Grundke Iqbal I" first="I." last="Grundke-Iqbal">I. Grundke-Iqbal</name><name sortKey="Iqbal, K" sort="Iqbal, K" uniqKey="Iqbal K" first="K." last="Iqbal">K. Iqbal</name><name sortKey="Wisniewski, M" sort="Wisniewski, M" uniqKey="Wisniewski M" first="M." last="Wisniewski">M. Wisniewski</name></country><country name="Suède"><noRegion><name sortKey="Bucht, G" sort="Bucht, G" uniqKey="Bucht G" first="G." last="Bucht">G. Bucht</name></noRegion><name sortKey="Winblad, B" sort="Winblad, B" uniqKey="Winblad B" first="B." last="Winblad">B. Winblad</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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