From a pathophysiological standpoint, APD consist of the “synucleinopaties”, such as MSA and DLB (with the common hallmark of soluble α-synuclein loss with corresponding insoluble α-synuclein accumulation), and “tauopathies” (characterized by soluble tau loss with corresponding insoluble tau accumulation), which include PSP and CBS [18,25]. The gene discussed is SNCA; the disease is tauopathy.