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Immunization of Tg-APPswe/PSEN1dE9 mice with Aβ3-10-KLH vaccine prevents synaptic deficits of Alzheimer’s disease

Bibliographic

Year of Publication:
2017
Contact PI Name:
YunPeng Cao
Contact PI Affiliation:
Department of Neurology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
Co-Authors:
Yuan Meng, Li Ding, HuiYi Zhang, WenChao Yin, Yi Yan
Primary Reference (PubMED ID):
Funding Source:
National Natural Science Foundation of China
Study Goal and Principal Findings:

The amyloid cascade hypothesis is widely accepted by researchers as the mechanism of Alzheimer’s disease. Active immunization to eliminate Aβ depositions has been used in preclinical and clinical studies. Aβ3-10-KLH is a vaccine of the Aβ3-10 peptide combined with keyhole limpet hemocyanin (KLH). They immunized 2.5-month old Tg-APPswe/PSEN1dE9 mice with Aβ3-10-KLH peptide and Aβ1-42 peptide to eliminate Aβ deposits in the brains of these transgenic mice. The results of immunohistochemical staining and transmission electron microscopy detection indicated that this new vaccine was more advantageous in protecting synaptic function and structure than the Aβ1-42 peptide. Aβ3-10-KLH peptide is an effective vaccine in the treatment of Alzheimer’s disease.

Therapeutic Agent

Therapeutic Information:
Therapy Type:
Biologic - Immunotherapy(active)
Therapeutic Agent:
Aβ3-10-KLH
Therapeutic Target:
beta Amyloid Peptide

Animal Model

Model Information:
Species:
Mouse
Model Type:
APPxPS1
Strain/Genetic Background:
B6C3

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
Histopathology
beta Amyloid Deposits
Synaptic Degeneration
Immunochemistry
Brain-beta Amyloid Deposits
Synaptophysin
Glutamate Ionotropic Receptor NMDA Type Subunit 2B (GluN2B/NR2B)
Electron Microscopy
Synaptic Density
Immunology
Antibody Titers
Pharmacodynamics
Target Engagement (Reduction beta Amyloid Peptides-Brain)