Similar to our previous findings in the fly AD model, we found reduced levels of AcH4K16 at all genes in all disease models, and reduced levels of AcH4K12 at all gene loci in all disease models except at sh. Together, these results suggest that disruption of Tip60 HAT homeostasis and concomitant epigenetic mediated neuroplasticity gene repression we previously observed in the AD brain is also an early common feature in PD, HD and ALS. Here, KAT5 is linked to Huntington disease.