Indeed, misfolded β-sheet-enriched proteins associated with neuronal deterioration—e.g., amyloid-β (Aβ) fragments, tau, α-synuclein (α-syn), polyglutamine (polyQ) expansion-containing proteins, and superoxide dismutase-1, implicated in Alzheimer’s disease (AD), tauopathies, Parkinson’s disease (PD), and Huntington’s disease (HD)/ataxia, respectively—and forming extra- or intra-cellular amyloids with cross β-pleated sheet conformation were reported to self-replicate, and are, therefore, increasingly denominated prions [31,32] or prion-like proteins. The gene discussed is MAPT; the disease is tauopathy.