While this may support a protective sequestrating activity of sPrP towards toxic protein assemblies, it confirms earlier findings in mouse models [71, 93] and provides a mechanistic rationale for the widespread earlier observation of “normal PrP” being enriched in extracellular protein deposits in diverse human proteinopathies [13, 31, 34–36, 84, 97, 100, 121]. This evidence concerns the gene PRNP and proteostasis deficiencies.