Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2002-05

AUTHORS

Jean-Cosme Dodart, Kelly R Bales, Kimberley S Gannon, Stephen J Greene, Ronald B DeMattos, Chantal Mathis, Cynthia A DeLong, Su Wu, Xin Wu, David M Holtzman, Steven M Paul

ABSTRACT

We have previously shown that chronic treatment with the monoclonal antibody m266, which is specific for amyloid beta-peptide (Abeta), increases plasma concentrations of Abeta and reduces Abeta burden in the PDAPP transgenic mouse model of Alzheimer's disease (AD). We now report that administration of m266 to PDAPP mice can rapidly reverse memory deficits in both an object recognition task and a holeboard learning and memory task, but without altering brain Abeta burden. We also found that an Abeta/antibody complex was present in both the plasma and the cerebrospinal fluid of m266-treated mice. Our data indicate that passive immunization with this anti-Abeta monoclonal antibody can very rapidly reverse memory impairment in certain learning and memory tasks in the PDAPP mouse model of AD, owing perhaps to enhanced peripheral clearance and (or) sequestration of a soluble brain Abeta species. More... »

PAGES

452-457

Journal

TITLE

Nature Neuroscience

ISSUE

5

VOLUME

5

Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nn842

    DOI

    http://dx.doi.org/10.1038/nn842

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/11941374


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