Alpha 1-Antichymotrypsin, an Inflammatory Protein Overexpressed in the Brains of Patients with Alzheimer’s Disease, Induces Tau Hyperphosphorylation through c-Jun N-Terminal Kinase Activation
Figure 1
Tau hyperphosphorylation in ACT expressing mice: cortex and hippocampal regions from normal nontransgenic (mTau), ACT expressing (ACT/mTau), human tau expressing (hTau), and both ACT and hTau expressing (ACT/mTau/hTau) mice were analyzed for changes in phosphorylation of tau at PHF-1 (a), p-Ser202 (b), pThr231 (c) specific epitopes, and total tau (d) using the corresponding P-tau or the TG5 total tau antibody by western blot and quantified using the Image J image analysis software. The data shows significant increase in P-tau levels in ACT and hTau as well as the double transgenic ACT/hTau mice (*). Only P-Ser202 tau showed significant change in double transgenic mice compared to mice expressing hTau alone (#).
