The current findings suggest that despite the relatively low levels of p-Tau in exosomes compared to the levels recovered from AD brain tissue, the p-Tau within the NDEVs could induce the templated misfolding of endogenous murine Tau and thereby transfer Tau pathology from the human samples to the mouse brain, wherein p-Tau pathology was propagated to un-injected areas. The gene discussed is MAPT; the disease is Alzheimer disease.