Abstract

Beta-amyloid peptide (AβP) aggregation, an essentially early event in Alzheimer's disease (AD) pathogenesis, became a target for therapeutics. We developed an immunization procedure, using as antigen the EFRH peptide located at the N-terminal region of AβP displayed on the filamentous phage, to raise anti-beta-amyloid peptide antibodies. Data demonstrated that a bacteriophage displaying different numbers of copies of self-epitope modulates the intensity of the immuno response. This immunization procedure led to improvement in cognitive functions and alleviated amyloid pathology in a transgenic mouse (Tg) model of AD.

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