While our finding that pTau accumulated together with upstream markers of pTau production (i.e., Dab1, pP85αTyr607) strongly suggests that pTau is locally produced by neurons within each affected region, it does not rule out the possibility that prion-like propagation of Tau, including pTau or Tau that is not detected by traditional methods [61, 82], could contribute to pTau-related neurodegeneration in sAD or other tauopathies. The gene discussed is DAB1; the disease is tauopathy.