In cellular studies, SIRT-2 inhibitors displayed different mechanisms in neuroprotection: in one study, γ-mangostin induced neurite outgrowth in an AD cellular model, [81,106] in another one, AGK2 reduced the reactive gliosis (which is considered one of the hallmarks of AD), [40] while in one other study, AK1 modulated mitochondrial dysfunction in AD cells, by recovering microtubule stabilization, and by eliminating toxic Aβ, thus improving cell survival [84,117]. This evidence concerns the gene AK1 and Alzheimer disease.