Fig. 6From: Neurons derived from sporadic Alzheimer’s disease iPSCs reveal elevated TAU hyperphosphorylation, increased amyloid levels, and GSK3B activationAnalysis of glycogen synthase kinase 3β (GSK3B) and the active form of GSK3B in neuronal culture. a Representative immunoblotting shows the phosphorylation of GSK3B at Ser9 (inactive form of the kinase [102]) and GSK3B in control neurons (ctrl-1), early-onset familial Alzheimer’s disease (fAD) neurons (fAD-1–fAD-4), and (b) sporadic Alzheimer’s disease (sAD) neurons (sAD-1–sAD-6) at all time points of neuronal terminal differentiation (TD14–TD70). c Quantification of the active GSK3B form at TD70 was presented as a percentage of nonphosphorylated GSK3B at Ser9. d Densitometric analysis of TAU phosphorylated at the T231 epitope at TD70. All values were normalized to GAPDH and are presented as mean ± SEM (n = 3). Dunnett’s test was performed to evaluate the significance of groups compared with control (*p < 0.05)Back to article page