APP and Alzheimer disease: Zhu et al. [128] have shown that overexpression of HDAC3 promotes Aβ levels and microglia activation, as well as reduces the density of dendritic spine in the hippocampus of APP/PS1 mice, while lentivirus-mediated inhibition of HDAC3 attenuates microglia activation and ameliorates cognition, as well as improves AD-related neuropathogenesis.