The molecular mechanisms remain to be fully clarified but it is suggested that a heterodimer of 3R and 4R tau with antiparallel β-sheet structure is initially generated and converts both 3R and 4R tau into amyloid-like PHFs in AD brain, while a homodimer of 3R or 4R tau with β-sheet structure converts only 3R or 4R tau into amyloid-like fibrils in 3R or 4R tauopathies, respectively [61]. The gene discussed is MAPT; the disease is tauopathy.