Affiliations: Institute of Neuroimmunology, Slovak Academy of Sciences, AD Centre, Dubravska, cesta, Bratislava, Slovak Republic
Correspondence:
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Correspondence to: Petr Novak, M.D, Dubravska cesta 9, 845 10 Bratislava, Slovak Republic. Tel.: +421 2 5477 8100; Fax: +421 2 5477 8100; E-mail: [email protected].
Abstract: 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.
Keywords: Alzheimer's disease, prions, tauons, tauopathies, truncated tau protein
