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A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease

BIBLIOGRAPHIC THERAPEUTIC AGENT ANIMAL MODEL EXPERIMENTAL DESIGN OUTCOMES

Bibliographic

Year of Publication:
2000
Contact PI Name:
Peter St. George-Hyslop
Contact PI Affiliation:
Centre for Research in Neurodegenerative Diseases, Departments of Medicine, Laboratory Medicine and Pathobiology, and Medical Biophysics, University of Toronto, Ontario, Canada
Co-Authors:
Christopher Janus, Jacqueline Pearson, JoAnne McLaurin, Paul M. Mathews, Ying Jiang, Stephen D. Schmidt, M. Azhar Chishti, Patrick Horne, Donna Heslin, Janet French, et al
Primary Reference (PubMED ID):
11140685
Funding Source:
Howard Hughes Medical Research Foundation
Alzheimer Society of Ontario
National Institute on Aging (NIA)
W. Garfeld Weston Foundation
Medical Research Council of Canada
Study Goal and Principal Findings:

The goal of this study was to determine the effects of Abeta  immunization on the AD-like behavioral deficits exhibited by TgCRND8 murine model of Alzheimer's disease. In summary the data showed that immunization of the TgCRND8 mouse model of AD with Abeta peptide 1-42 reduced both deposition of cerebral fibrillar Abeta and cognitive dysfunction, without altering total levels of Abeta peptide in the brain. The data imply that either a approximately 50% reduction in dense-cored Abeta plaques is sufficient to affect cognition, or that vaccination modulates the activity/abundance of a small subpopulation of especially toxic Abeta species.These data support the hypotheses that Abeta plays a central role in Alzheimer's disease and that procedures that modulate its production, assembly and/or removal might be used as treatments.

Bibliographic Notes:
Full Author List: Christopher Janus, Jacqueline Pearson, JoAnne McLaurin, Paul M. Mathews, Ying Jiang, Stephen D. Schmidt, M. Azhar Chishti, Patrick Horne, Donna Heslin, Janet French, Howard T.J. Mount, Ralph A. Nixon, Marc Mercken, Catherine Bergeron, Paul E. Fraser, Peter St. George-Hyslop and David Westaway.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Biologic - Immunotherapy(active)
Therapeutic Agent:
beta Amyloid Peptide 1-42
PubMed
PubChem
ClinicalTrials
Patents
Therapeutic Target:
beta Amyloid Peptide
Open Targets
Pharos
Agora

Animal Model

Model Information:
Species:
Mouse
Model Type:
APP
Model Name:
TgCRND8
ALZFORUM
Strain/Genetic Background:
Hybrid C3H/BL/6

Experimental Design

Is the following information reported in the study?:
Power/Sample Size Calculation
Randomized into Groups
Blinded for Treatment
Blinded for Outcome Measures
Pharmacokinetic Measures
Pharmacodynamic Measures
Toxicology Measures
ADME Measures
Biomarkers
Dose
Formulation
Route of Delivery
Duration of Treatment
Frequency of Administration
Age of Animal at the Beginning of Treatment
Age of Animal at the End of Treatment
Sex as a Biological Variable
Study Balanced for Sex as a Biological Variable
Number of Premature Deaths
Number of Excluded Animals
Statistical Plan
Genetic Background
Inclusion/Exclusion Criteria Included
Conflict of Interest

Outcomes

Outcome Measured
Outcome Parameters
Behavioral
Morris Water Maze
Histopathology
beta Amyloid Load
Dense-core/Compact Plaques
Biochemical
Brain-beta Amyloid Peptide-Total
Immunology
Anti-beta Amyloid Antibody Titers
Pharmacodynamics
Target Engagement (Binding beta Amyloid Antibodies to beta Amyloid Deposits)
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