. Therapeutic effects of PKC activators in Alzheimer's disease transgenic mice. Proc Natl Acad Sci U S A. 2004 Jul 27;101(30):11141-6. PubMed.

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  1. This interesting paper shows that the PKC activator bryostatin, currently investigated in humans as an anti-cancer agent, enhances alpha-secretase cleavage of APP, presumably at the expense of beta-secretase cleavage, and reduces the production of Abeta in transgenic mouse models of AD. The paper raises some interesting questions, to which it would be informative to have answers:

    Does bryostatin have neuroprotective properties?

    If it does, is the neuroprotection due to altered processing of APP or to modulation of a signal transduction pathway mediated by PKC?

    Given that bryostatin treatment reduced Abeta in transgenic mouse models, why did it not have an effect on cognition? Do the data suggest a lack of correlation between the production of Abeta and impairment of cognition?

  2. I have some difficulty to understand this paper. There are no data of bryostatin on APP V717I mutated mice. For the other model, APP(V717I)/PS1 (A246E), the study presents data on mortality, but not on the number of amyloid plaques, nor on the secretion of sAPPalpha and cognition.

    Therefore this paper offers many different (and unrelated) stories followed by a unifying conclusion that I have some difficulty to believe.

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