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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Nasal vaccination with a proteosome-based adjuvant and glatiramer acetate clears
β-amyloid in a mouse model
of Alzheimer disease</title><author><name sortKey="Frenkel, Dan" sort="Frenkel, Dan" uniqKey="Frenkel D" first="Dan" last="Frenkel">Dan Frenkel</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author><author><name sortKey="Maron, Ruth" sort="Maron, Ruth" uniqKey="Maron R" first="Ruth" last="Maron">Ruth Maron</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author><author><name sortKey="Burt, David S" sort="Burt, David S" uniqKey="Burt D" first="David S." last="Burt">David S. Burt</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">ID Biomedical Corporation of Quebec, Laval, Quebec, Canada.</nlm:aff></affiliation></author><author><name sortKey="Weiner, Howard L" sort="Weiner, Howard L" uniqKey="Weiner H" first="Howard L." last="Weiner">Howard L. Weiner</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">16100572</idno><idno type="pmc">1184038</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1184038</idno><idno type="RBID">PMC:1184038</idno><idno type="doi">10.1172/JCI23241</idno><date when="2005">2005</date><idno type="wicri:Area/Pmc/Corpus">000216</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000216</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Nasal vaccination with a proteosome-based adjuvant and glatiramer acetate clears
β-amyloid in a mouse model
of Alzheimer disease</title><author><name sortKey="Frenkel, Dan" sort="Frenkel, Dan" uniqKey="Frenkel D" first="Dan" last="Frenkel">Dan Frenkel</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author><author><name sortKey="Maron, Ruth" sort="Maron, Ruth" uniqKey="Maron R" first="Ruth" last="Maron">Ruth Maron</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author><author><name sortKey="Burt, David S" sort="Burt, David S" uniqKey="Burt D" first="David S." last="Burt">David S. Burt</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">ID Biomedical Corporation of Quebec, Laval, Quebec, Canada.</nlm:aff></affiliation></author><author><name sortKey="Weiner, Howard L" sort="Weiner, Howard L" uniqKey="Weiner H" first="Howard L." last="Weiner">Howard L. Weiner</name><affiliation><nlm:aff id="N0x8b767e0.0x9d61c68">Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.</nlm:aff></affiliation></author></analytic><series><title level="j">Journal of Clinical Investigation</title><idno type="ISSN">0021-9738</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Amyloid β-peptide (Aβ) appears to play a key pathogenic role in Alzheimer disease (AD). Immune therapy in mouse models of AD via Aβ immunization or passive administration of Aβ antibodies markedly reduces Aβ levels and reverses behavioral impairment. However, a human trial of Aβ immunization led to meningoencephalitis in some patients and was discontinued. Here we show that nasal vaccination with a proteosome-based adjuvant that is well tolerated in humans plus glatiramer acetate, an FDA-approved synthetic copolymer used to treat multiple sclerosis, potently decreases Aβ plaques in an AD mouse model. This effect did not require the presence of antibody, as it was observed in B cell–deficient (<italic>Ig</italic> μ<italic>–null</italic>) mice. Vaccinated animals developed activated microglia that colocalized with Aβ fibrils, and the extent of microglial activation correlated strongly with the decrease in Aβ fibrils. Activation of microglia and clearing of Aβ occurred with the adjuvant alone, although to a lesser degree. Our results identify a novel approach to immune therapy for AD that involves clearing of Aβ through the utilization of compounds that have been safely tested on or are currently in use in humans.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Invest</journal-id><journal-id journal-id-type="publisher-id">J CLIN INVEST</journal-id><journal-title>Journal of Clinical Investigation</journal-title><issn pub-type="ppub">0021-9738</issn><publisher><publisher-name>American Society for Clinical Investigation</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">16100572</article-id><article-id pub-id-type="pmc">1184038</article-id><article-id pub-id-type="publisher-id">23241</article-id><article-id pub-id-type="doi">10.1172/JCI23241</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Nasal vaccination with a proteosome-based adjuvant and glatiramer acetate clears
β-amyloid in a mouse model
of Alzheimer disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Frenkel</surname><given-names>Dan</given-names></name><xref ref-type="aff" rid="N0x8b767e0.0x9d61c68">1</xref></contrib><contrib contrib-type="author"><name><surname>Maron</surname><given-names>Ruth</given-names></name><xref ref-type="aff" rid="N0x8b767e0.0x9d61c68">1</xref></contrib><contrib contrib-type="author"><name><surname>Burt</surname><given-names>David S.</given-names></name><xref ref-type="aff" rid="N0x8b767e0.0x9d61c68">2</xref></contrib><contrib contrib-type="author"><name><surname>Weiner</surname><given-names>Howard L.</given-names></name><xref ref-type="aff" rid="N0x8b767e0.0x9d61c68">1</xref></contrib></contrib-group><aff id="N0x8b767e0.0x9d61c68"><label>1</label>Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA.<label>2</label>ID Biomedical Corporation of Quebec, Laval, Quebec, Canada.</aff><author-notes><fn><p>Address correspondence to: Howard L. Weiner, Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Harvard Institute of Medicine 730, Boston, Massachusetts 02115, USA. Phone: (617) 525-5300; Fax: (617) 525-5252; E-mail: <email>hweiner@rics.bwh.harvard.edu</email>.</p></fn></author-notes><pub-date pub-type="ppub"><day>1</day><month>9</month><year>2005</year></pub-date><pub-date pub-type="epub"><day>11</day><month>8</month><year>2005</year></pub-date><volume>115</volume><issue>9</issue><fpage>2423</fpage><lpage>2433</lpage><history><date date-type="received"><day>2</day><month>9</month><year>2004</year></date><date date-type="accepted"><day>7</day><month>6</month><year>2005</year></date></history><copyright-statement>Copyright © 2005, American Society for Clinical Investigation</copyright-statement><copyright-year>2005</copyright-year><abstract><p>Amyloid β-peptide (Aβ) appears to play a key pathogenic role in Alzheimer disease (AD). Immune therapy in mouse models of AD via Aβ immunization or passive administration of Aβ antibodies markedly reduces Aβ levels and reverses behavioral impairment. However, a human trial of Aβ immunization led to meningoencephalitis in some patients and was discontinued. Here we show that nasal vaccination with a proteosome-based adjuvant that is well tolerated in humans plus glatiramer acetate, an FDA-approved synthetic copolymer used to treat multiple sclerosis, potently decreases Aβ plaques in an AD mouse model. This effect did not require the presence of antibody, as it was observed in B cell–deficient (<italic>Ig</italic> μ<italic>–null</italic>) mice. Vaccinated animals developed activated microglia that colocalized with Aβ fibrils, and the extent of microglial activation correlated strongly with the decrease in Aβ fibrils. Activation of microglia and clearing of Aβ occurred with the adjuvant alone, although to a lesser degree. Our results identify a novel approach to immune therapy for AD that involves clearing of Aβ through the utilization of compounds that have been safely tested on or are currently in use in humans.</p></abstract></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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