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Vol. 2, No. 5, 2005
Issue release date: February 2006
Section title: Special Topic Section: Immunotherapies and Related Strategies in Alzheimer’s ...
Neurodegenerative Dis 2005;2:261–266
(DOI:10.1159/000090366)

Mechanisms of Aβ Plaque Clearance following Passive Aβ Immunization

Morgan D.
Alzheimer Research Laboratory, Department of Pharmacology, University of South Florida, Tampa, Fla., USA

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Article / Publication Details

First-Page Preview
Abstract of Special Topic Section: Immunotherapies and Related Strategies in Alzheimer’s ...

Published online: 2/22/2006

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD

Abstract

Alzheimer’s disease is a major health problem with limited available medical treatment options. Immunotherapy is one approach with the potential to slow or reverse the disease process. In transgenic mouse models of amyloid deposition, anti-Aβ immunotherapy is remarkably effective at diminishing the amyloid burden and reversing the memory deficiency phenotype present in these mice. Three distinct mechanisms of antibody action have been proposed to mediate these benefits of anti-Aβ immunotherapy. The first is a catalytic dissolution of the Aβ fibrils, proposed by Beka Solomon and colleagues. A second mechanism is opsonization of the amyloid by the antibody and subsequent phagocytosis by macrophages proposed by Dale Schenk and the Elan group. A third mechanism proposed by DeMattos, Holtzman and colleagues is the peripheral sink hypothesis, arguing that circulating antibodies sequester Aβ and favor efflux of Aβ from the CNS over influx to the CNS. None of these mechanisms are mutually exclusive. Our research group has evaluated these mechanisms using intracranial injection and systemic administration of anti-Aβ antibodies. We found evidence supporting all three mechanisms, and suggest they may act synergistically to achieve the large effect size of the immunotherapeutic approach. However, in aged amyloid precursor protein transgenic mice administered anti-Aβ antibodies systemically, there is a redistribution of the amyloid from the parenchyma to vascular elements. This increase in congophilic angiopathy is associated with increased risk of microhemorrhage. Thus, although we favor continued testing of the immunotherapy to treat Alzheimer’s disease, we believe caution should be taken to minimize the risk of vascular leakage.


  

Author Contacts

Dave Morgan
College of Medicine, University of South Florida
12901 Bruce Downs Blv/MDC Box 9
Tampa, FL 33612-4799 (USA)
Tel. +1 813 974 3949, Fax +1 813 974 2565, E-Mail dmorgan@hsc.usf.edu

  

Article Information

Received: April 15, 2005
Accepted after revision: May 18, 2005
Number of Print Pages : 6
Number of Figures : 3, Number of Tables : 0, Number of References : 14

  

Publication Details

Neurodegenerative Diseases

Vol. 2, No. 5, Year 2005 (Cover Date: February 2006)

Journal Editor: Nitsch, R.M. (Zürich)
ISSN: 1660–2854 (print), 1660–2862 (Online)

For additional information: http://www.karger.com/NDD


Article / Publication Details

First-Page Preview
Abstract of Special Topic Section: Immunotherapies and Related Strategies in Alzheimer’s ...

Published online: 2/22/2006

Number of Print Pages: 6
Number of Figures: 3
Number of Tables: 0

ISSN: 1660-2854 (Print)
eISSN: 1660-2862 (Online)

For additional information: http://www.karger.com/NDD


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in goverment regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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