On the other hand, elevated HDAC2 levels are involved in the cognitive decline associated with neurodegeneration in CK-p25 mice, through mechanisms involving glucocorticoid receptor 1 (GR1) phosphorylation and interaction with the HDAC2 promoter-glucocorticoid response elements (GRE), whereas the prevention of HDAC2 upregulation rescues memory capacities in a model Alzheimer’s disease [25]. Here, HDAC2 is linked to early-onset autosomal dominant Alzheimer disease.