Nuclear translocation of class II HDACs such as HDAC4 and HDAC6 is regulated by Aβ oligomers and the apolipoprotein E ε4 allele (apoE4), which is a critical AD risk factor, resulting in the downregulation of BDNF expression, which is important for controlling synaptic repair and synaptic plasticity82. Here, APOE is linked to Alzheimer disease.