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Fig. 4 | Acta Neuropathologica Communications

Fig. 4

From: Upregulation of calpain activity precedes tau phosphorylation and loss of synaptic proteins in Alzheimer’s disease brain

Fig. 4

Changes in cdk5 and GSK-3 activities with AD progression. a Representative blots of cortical homogenates from postmortem brain. Blots were probed with antibodies against cyclin dependent kinase 5 (cdk5) to detect holoprotein at 33 kDa, p35 to detect holoprotein at 35 kDa and calpain-cleaved 25 kDa fragments (p25) at 25 kDa, total glycogen synthase kinase 3α/β (totGSK3) at 47 and 51 kDa, respectively and GSK3α/β phosphorylated at Ser21/9 (pGSK3). Blots were also probed with an antibody against neuron-specific enolase (NSE, 45 kDa) as a loading control. Bar graphs show amounts of (b) cdk5 relative to NSE, (c) p35 following normalisation to cdk5,  (d) the p25/p35 ratio, (e) GSK3α and (f) GSK3β relative to NSE, and (g) phosphorylated (inactive) GSK3 normalised to total GSK-3 protein. CTRL: control (n = 5), Braak II AD (n = 4), Braak III AD (n = 3), Braak IV AD (n = 4), Braak V AD (n = 3), Braak VI AD (n = 5). Data is mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001

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