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Fasting is required for CR-induced improvements in tau hyperphosphorylation and neuroinflammation, but not for CR-induced improvements in A plaque deposition To investigate the role of fasting in the ability of CR to attenuate AD pathology, we evaluated several pathological hallmarks of AD, including phosphorylation of tau, amyloid beta (A) plaque deposition, and gliosis
In addition, we treated PC cells with monensin to make SLC7A11 remain in Golgi and trace its expression upon monensin removal
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Design of in vivo Experiments The animals were separated into 4 groups according to the treatment schedule, as follows: saline (saline 0.9% + cecal ligation and puncture CLP/ n = 18 animals), Ceftriaxone (Cef 20 mg/kg + CLP/ n = 6 animals), aqueous extract of Ab (Ab 135 mg/kg + CLP, n = 18 animals) and sham (surgery control, n = 18 animals)
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