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Swiss Medical Weekly
Compelling evidence from the last three decades clearly shows that transmissible spongiform encephalopathies (TSEs) develop as a result of a poorly understood misfolding event that converts the cellular prion protein (PrP C ) to an isoform known as PrP Sc which is aggregated, protease resistant and able to impose its aberrant conformation onto PrP C , leading to its accumulation in the central nervous system. Despite all the knowledge gathered in more than thirty years of research and thedoi:10.4414/smw.2016.14354 pmid:27684312 fatcat:touga77vzzefbngna5l533areq