The paradigm of Alzheimer's disease (AD) is one subject to frequent change: what was thought to be a rare form of pre-senile dementia was revealed as a wide-spread malady; where amyloid-β was deemed the sole causative agent for the better part of 20 years, tau protein was shown to play a crucial role in AD genesis. With the discovery of possible prion-like phenomena in this disease supposedly driven by cell-autonomous processes, an evaluation of the similarities and differences between tau-driven neurodegeneration and prion disease becomes necessary. In this article, we provide a comparison of the template agent genesis, filament assembly, as well as intra- and inter-individual spread of prions and tauons.