. Immunization with a nontoxic/nonfibrillar amyloid-beta homologous peptide reduces Alzheimer's disease-associated pathology in transgenic mice. Am J Pathol. 2001 Aug;159(2):439-47. PubMed.


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  1. The data in the paper by Sigurdsson et al. are convinced that the immunization
    protocol they used is effective in decreasing plaque burden in the Tg2576 (also
    called APPsw) mouse model of AD. They present nice evidence that the peptide
    with which they immunized the mice does not become fibrillar in the assays they
    used. This is important as it makes it likely that the antibodies generated
    by the immunized mice are likely to be recognizing soluble and not just insoluble
    forms of Aβ very well.

    If immunization ends up being a treatment to prevent or treat AD, it is not
    yet clear whether immunizing with soluble or fibrillar forms or Aβ will
    be better in humans. Sigurdsson, et al., bring up the possible advantages of utilizing
    a soluble, nontoxic fragment of Aβ. Whether or not these potential advantages
    turn out to be correct, their work is important because it simply is not clear
    yet, until trials are done in humans, which of the immunization protocols will
    not only be effective but also demonstrate the least toxicity.

    View all comments by David Holtzman
  2. This provides further confirmation of the value of immunization in reducing amyloid burden.

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