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Part of the book series: Research and Perspectives in Alzheimer’s Disease ((ALZHEIMER))

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Summary

A beta amyloid (Aβ) peptide vaccine can decrease brain Aβ deposition as well as partially protect against memory loss in a transgenic mouse model for Alzheimer’s Disease (AD) that expresses human amyloid precursor protein (APP) and presenilin-1 (PS-1). Current information indicates that antibodies elicited by this vaccine probably mediate the protective effect, although the precise mechanism of action for these antibodies has not yet been established. One of our major interests has been the more extensive characterization of the Aβ vaccine, as well as developing methods for optimizing and maximizing this vaccine strategy. Optimization is important since we have observed that at least three vaccinations with the Aβ peptide vaccine were needed to elicit a significant antibody response. Also, a less robust antibody response to the Aβ vaccine was noted in older animals (i.e., 23 months of age) than in younger animals (4 and 15 months of age).

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Correspondence to K. E. Ugen .

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© 2003 Springer-Verlag Berlin Heidelberg

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Cao, C. et al. (2003). Characterization of Amyloid Beta Vaccination Strategies in Mice. In: Selkoe, D.J., Christen, Y. (eds) Immunization Against Alzheimer’s Disease and Other Neurodegenerative Disorders. Research and Perspectives in Alzheimer’s Disease. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59332-1_3

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  • DOI: https://doi.org/10.1007/978-3-642-59332-1_3

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-642-63937-1

  • Online ISBN: 978-3-642-59332-1

  • eBook Packages: Springer Book Archive

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