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2.7.11.31

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20180906

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Interestingly, treatment with Ab42 decreased the phosphorylation of AMPK at Thr172, whereas the total amount of AMPK was not altered in primary cortical neurons PubMed:22419736

We found, in addition, that enzyme activity of AMPK was sup- pressed in the cortical neurons after exposure to Ab42 PubMed:22419736

These results indicate that AMPK activity is impaired by Ab42 in the neuronal cells in which tau phosphor- ylation increased. PubMed:22419736

Conversely, treatment with AICAR (5-aminoimidazole-4- carboxamide ribonucleoside), an AMPK activator (34), increased the inhibitory phosphorylation of GSK3b and reduced tau phosphorylation at Ser396/404 in SH-SY5Y cells and cortical neurons PubMed:22419736

As shown in Figure 5A and B, treatment of control cells with Ab42 reduced the levels of AMPK phosphorylation at Thr172 and the inhibitory phosphorylation of GSK3b at Ser9. On the contrary, these alterations triggered by Ab42 were not observed in SH-SY5Y/AK1 knockdown cells, showing no changes in the levels of the phosphorylated AMPK and GSK3b. These results suggest that AK1 plays a crucial role in the regulation of AMPK and GSK3b in the neuronal cells exposed to Ab42. PubMed:22419736

These results indicate that AMPK activity is impaired by Ab42 in the neuronal cells in which tau phosphor- ylation increased. PubMed:22419736

AK1 overexpression markedly decreased AMPK phosphorylation at Thr172 in the primary neurons, whereas AK1 R132A mutant failed to do so PubMed:22419736

These results indicate that AMPK activity is impaired by Ab42 in the neuronal cells in which tau phosphor- ylation increased. PubMed:22419736

The treatment of cortical neurons with compound C, a selective AMPK inhibitor (33), reduced the inhibitory phosphorylation of GSK3b at Ser9 and markedly increased tau phosphorylation at Ser396/404 PubMed:22419736

Conversely, treatment with AICAR (5-aminoimidazole-4- carboxamide ribonucleoside), an AMPK activator (34), increased the inhibitory phosphorylation of GSK3b and reduced tau phosphorylation at Ser396/404 in SH-SY5Y cells and cortical neurons PubMed:22419736

The treatment of cortical neurons with compound C, a selective AMPK inhibitor (33), reduced the inhibitory phosphorylation of GSK3b at Ser9 and markedly increased tau phosphorylation at Ser396/404 PubMed:22419736

Conversely, treatment with AICAR (5-aminoimidazole-4- carboxamide ribonucleoside), an AMPK activator (34), increased the inhibitory phosphorylation of GSK3b and reduced tau phosphorylation at Ser396/404 in SH-SY5Y cells and cortical neurons PubMed:22419736

The treatment of cortical neurons with compound C, a selective AMPK inhibitor (33), reduced the inhibitory phosphorylation of GSK3b at Ser9 and markedly increased tau phosphorylation at Ser396/404 PubMed:22419736

Conversely, treatment with AICAR (5-aminoimidazole-4- carboxamide ribonucleoside), an AMPK activator (34), increased the inhibitory phosphorylation of GSK3b and reduced tau phosphorylation at Ser396/404 in SH-SY5Y cells and cortical neurons PubMed:22419736

These observations indicate that AMPK negatively regulates GSK3b activity and tau phosphorylation PubMed:22419736

These observations indicate that AMPK negatively regulates GSK3b activity and tau phosphorylation PubMed:22419736