In agreement with these results, studies using tauopathy or Aβ plaque models for Alzheimer’s disease showed that pharmacological inhibition of HDAC6 rescues axonal transport and some features of the Alzheimer’s disease phenotype, e.g., spatial memory deficits, as well as hippocampal synapse loss, possibly through HDAC6 interaction with Tau [362,363,377,378,379,380]. This evidence concerns the gene HDAC6 and early-onset autosomal dominant Alzheimer disease.