SIRT1 Regulates Cognitive Performance and Ability of Learning and Memory in Diabetic and Nondiabetic Models

Figure 1

Deacetylation of SIRT1 in cognition and learning and memory. Increased SIRT1 level may reduce the production of ROS, Aβ, and p-tau, as well as promote neuronal survival and dendritic growth, contributing to improve learning and memory. ADAM10: a disintegrin and metalloprotease 10; AMPK: adenosine monophosphate-activated protein kinase; p-ERK: phosphorylated extracellular signal-regulated kinase; p-GSK3β: phosphorylated glycogen synthesis kinase 3 beta; p-JNK: phosphorylated Jun-terminal kinase; Ac-NFκβ: acetylated nuclear factor-kappa beta; Ac-FoxO1: acetylated the forkhead box subgroup O 1; Ac-p53: acetylated p53; HSP70: heat shock protein 70; mTOR: mammalian target of rapamycin; p70S6K: p70S6 kinase; PGC-1α: peroxisome proliferator-activated receptor γ transcriptional coactivator 1-α; ROCK: Rho-associated protein kinase; JNK: Jun N-terminal kinase; Aβ: amyloid beta; ROS: reactive oxygen species; p-tau: phosphorylated tau.