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]. The gene discussed is HDAC6; the disease is Alzheimer disease.