Such a repressor function of HDAC2 was also shown in p25 transgenic animals modeling Alzheimer’s disease [399], in which an increase in the level of this histone deacetylase isoform correlated with cognitive deficits due to the higher recruitment of HDAC2 on the promoters of key genes associated with learning, memory, and neuroplasticity when compared with wild-type animals. This evidence concerns the gene HDAC2 and early-onset autosomal dominant Alzheimer disease.