ANALYSIS OF TAU PROTEIN IN EXOSOMES AND MICROVESICLES ISOLATED FROM A MOUSE MODEL OF ALZHEIMER'S DISEASE

a consistent result with in vivo findings of that the pharmacological activation of AMPK by AICAR inhibited the phosphorylation of Tau-Ser396, but increased the phosphorylation of Tau-Ser262.The reduced expression of SIRT1 and the increased expression of p-AMPK in the cortex of SAMP8 5 months group were also observed, as compared to same aged SAMR1 group. These results implicate that AMPK activation may be caused by reduced expression of SIRT1, and which may differentially regulate the phosphorylation of tau protein. Conclusions: A novel finding of significant suppression of SIRT1 and the concomitant increased activity of AMPK in the cortex of SAMP8 aged 2 months without increment of APP expressionis reported. In addition, we found that AMPK activation induce a differential phosphorylation of tau protein in vitro and in vivo models. In conclusion, further investigations are planned to test the hypothesis that the SIRT1 inhibition followed by AMPK activation may be one of the pathogenic mechanisms of tau-related neurodegeneration.