Since histone acetylation-mediated epigenetic control is highly dynamic, it was also determined that a knock-down of HDAC2 [115] or treatment with diverse HDAC inhibitors targeting HDAC2 [113,116,117] rescues pathologic cognitive deficits in AD mice, promoting neuroplasticity-related gene expression, reinstating morphological alterations and synaptic plasticity and restoring memory deficits. Here, HDAC9 is linked to Alzheimer disease.