Target Validation Studies of PS48, a PDK-1 Allosteric Agonist, for the Treatment of Alzheimer's Disease Phenotype in APP/PS1 Transgenic Mice.

When the IP Akt was added to an in vitro reaction with an added GSK3-β consensus peptide-fusion (crosstide, MW 20 kDa) as a substrate, we saw that Akt activity in TG mice was suppressed by ~25%, just short of significance ( p = 0.05).

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In plaque-free zones of the PFC and hippocampus, while basal pAkt was significantly inhibited in TG mice, as expected, PS48 had no effect save for a positive trend in the PFC of animals fed an SD.

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For instance, crude lysates from TG animals on a SD showed only a small trend in pAkt/totAkt ratio change, still favoring PS48 ( Supplement Figure S1A ), whereas the difference was more noticeable when first immunoprecipitated ( Figure 1 A).

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Under standard diet—SD—conditions, the improvement from basal levels with PS48 was a trend that did not quite reach statistical significance ( Figure 1 A) but did adjust to a level that was not significantly different from wild-type—WT—control.

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