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Fig. 6 | Alzheimer's Research & Therapy

Fig. 6

From: Neurons derived from sporadic Alzheimer’s disease iPSCs reveal elevated TAU hyperphosphorylation, increased amyloid levels, and GSK3B activation

Fig. 6

Analysis 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)

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