Almost all published studies that examined
ABT737 Aβ levels using possible modulators did not compare AD transgenic mice with their wild-type littermates. In these studies, the plasma Aβ concentration was compared with either the plasma Aβ level at baseline or the Aβ level in vehicle-treated transgenic mice [4]. It would be important to be able to differentiate the plasma Aβ level in AD patients compared to that in non-demented controls, to be an ideal diagnostic tool for AD. In this present study, we compared AD transgenic mice to their wild-type littermates, and observed a significant difference in the magnitude of the increase in plasma Aβ level after
glucose loading between genotypes. Importantly, this difference was observed even in the very early stage of disease (as early as 3 months of age). However, it should be considered that our results based on transgenic mice with familial AD mutations implicate this phenomenon only in individuals with a genetic tendency of developing AD. It would be important to evaluate the possible effects of glucose loading on plasma Aβ in sporadic AD cases.
