. 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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