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Therefore, based on the mechanisms described above, therapeutic strategies could be to block C3 production at the source, for example, by applying a TLR2‐specific antagonist (e.g., C29) or an NF‐κB inhibitor (JSH‐23), and to interrupt C3‐C3aR signaling, for example, by using a C3aR antagonist (SB290157) treatment attenuates tau hyperphosphorylation through the GSK3β signaling pathway and inhibits neuronal apoptosis

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3) sirtuins, main sensors for nutrient state, are activated by increased NAD + /NADH ratio 12