. In vitro characterization of Pittsburgh compound-B binding to Lewy bodies. J Neurosci. 2007 Sep 26;27(39):10365-71. PubMed.


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  1. Besides the interesting issues already discussed at length and in depth, the data bring to mind the problem of why N-terminally directed antibodies—and particularly those against the EFRH epitope as demonstrated by Beka Solomon and coworkers—are most efficient in passive vaccination. The explanation is that the N-terminal is "dangling" outside the amyloid fibers and thereby accessible.

    Then I wonder about antibodies that react about two orders of magnitude less well with pE-Aβ (i.e., Aβ3-42 peptide, starting with pyroglutamyl at residue Glu-3), than with wt-Aβ (Gardberg et al., 2007). Are these acting not or less well on pE-Aβ in human brain and thereby explaining differences in efficacy of passive vaccination in mouse models and human patients?


    . Molecular basis for passive immunotherapy of Alzheimer's disease. Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15659-64. PubMed.

    View all comments by Fred Van Leuven

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