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Reduced effectiveness of Abeta1-42 immunization in APP transgenic mice with significant amyloid deposition.

P Das¹, M P Murphy, L H Younkin

¹Department of Neurosciences, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, Florida 32224, USA.

Neurobiology of Aging

|November 14, 2001

Summary

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Abeta1-42 immunization effectively reduces amyloid burden in early stages of Alzheimer's disease (AD) models. However, it shows limited efficacy in clearing pre-existing amyloid deposits in established AD.

Area of Science:

Neuroscience
Immunology
Pathology

Background:

Alzheimer's disease (AD) is characterized by amyloid-beta (Abeta) plaque accumulation.
Abeta1-42 vaccinations have shown promise in reducing amyloid burden in AD models.

Purpose of the Study:

To evaluate the efficacy of Abeta1-42 immunization in the Tg2576 mouse model of AD at different stages of amyloid deposition.
To determine if Abeta1-42 immunization can clear pre-existing amyloid plaques.

Main Methods:

Tg2576 mice were immunized with Abeta1-42 at stages of minimal, modest, and significant amyloid deposition.
Biochemical and immunohistochemical methods were used to assess Abeta deposition and plaque load.

Main Results:

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Immunization prior to significant amyloid deposition effectively reduced both Abeta40 and Abeta42 levels and plaque load.

Immunization with modest pre-existing deposits reduced Abeta42 but not Abeta40, with reduced plaque load.

Immunization in mice with significant amyloid burden showed minimal reduction in Abeta42 and no change in Abeta40 or plaque load.

Conclusions:

Abeta1-42 immunization is most effective at preventing further Abeta accumulation when administered early in the disease process.
Abeta1-42 immunization does not significantly clear established amyloid deposits in the Tg2576 mouse model.