HDAC2 histone deacetylases may be the ultimate target enzymes that need to be inhibited in the brain of Alzheimer's patients, hyppocampus especially where the new memory is formed. They inhibit the expression of genes involved in synaptic plasticity by inducing the closed chromatin conformation in the regions of these genes. By inhibiting HDAC2 in mice with AD symptoms, researchers were able to restore their cognitive functions. The formation of amyloid plaques thus seems not be the leading cause of AD.
This also raises another question whether AD is epigentically regulated in any way. If this is the case, it would implicate that environmental stimuli in early development of an oocite would poise the future events and lead to development of AD in the later stages of life, and also maybe in a subsequent generation.