FIGURE 2.

Aβ treatment promotes biochemical changes, suggesting inactivation of Akt and Erk1/2 and activation of Tau-targeting kinases GSK3β and Cdk5. A, shown are immunoblots of the survival kinase Akt and its activated form, phospho-Akt at serine 473 (pAkt (473)). B, shown are immunoblots of Erk1/2 and its activated form, phospho-Erk1/2. C, shown are immunoblots of GSK3β and an inactivated form, phospho-GSK3β, at serine 9 (pGSK3β (9)). D, shown are immunoblots of p35 and the production of its proteolytic fragment, p25 (an activator of Cdk5). Panels A–D graphically present densitometry analysis (above) of the respective protein levels determined by immunoblotting (below). For each time point we first normalize the GAPDH data from the untreated (−) and treated (+) samples. Using this correction factor, we then ratio the Aβ treated versus untreated signals for each band of interest to generate the -fold intensity of each treated time point (shown in the bar graphs). Error bars represent S.E. of densitometry from three independent experiments. E, shown is a graphic summary of the data in A–D. Cdk5 activity is suggested by p25 fragment production. Non-phospho-GSK3β (npGSK3β) indicates the loss of signal for phospho-GSK3β at serine 9, suggesting activation of this kinase. Kinases in black are graphed against the left y axis, whereas kinases in gray are graphed against the right y axis. Note that the x axis is non-linear. Error bars represent S.E. of densitometry from 3 independent experiments.