Below, we first provide context (Section 3.1) via a brief description of classic prions, highlighting (i) the template misfolding of proteins and amyloidosis; (ii) the spreading of the misfolding in a non-cell-autonomous manner (promoting disease progression); and (iii) the existence of prion strains that can account for disparate disease outcomes, despite the shared root cause of misfolding one particular species of protein (e.g., misfolded prion protein causes various diseases; misfolded tau causes various distinct tauopathies). Here, MAPT is linked to tauopathy.