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First, prion diseases, in addition to being sporadic or genetic like all other neurodegenerative diseases, are infectious diseases. Animal models were developed early on (a long time before the advent of transgenic technology), and this has made possible the discovery of the prion protein as the infectious agent. Second, human prion diseases have true equivalents in animals, such as scrapie, which has been the subject of experimental research for many years. Variant <jats:styled-content style=\"fixed-case\">C<\/jats:styled-content>reutzfeldt\u2013<jats:styled-content style=\"fixed-case\">J<\/jats:styled-content>akob disease (vCJD) is a zoonosis caused by bovine spongiform encephalopathy (<jats:styled-content style=\"fixed-case\">BSE<\/jats:styled-content>) prions. Third, they show a wide variety of phenotypes in humans and animals, much wider than the variants of any other sporadic or genetic neurodegenerative disease. It has now become firmly established that particular PrP<jats:sup>Sc<\/jats:sup> isoforms are closely related to specific human prion strains. The variety of human prion diseases, still an enigma in its own right, is a focus of this article. Recently, a series of experiments has shown that the concept of aberrant protein folding and templating, first developed for prions, may apply to a variety of neurodegenerative diseases. In the wake of these discoveries, the term prion has come to be used for A\u03b2, \u03b1\u2010synuclein, tau and possibly others. The self\u2010propagation of alternative conformations seems to be the common denominator of these \u201cprions,\u201d which in future, in order to avoid confusion, may have to be specified either as \u201cneurodegenerative prions\u201d or \u201cinfectious prions.\u201d<\/jats:p>","DOI":"10.1111\/bpa.12045","type":"journal-article","created":{"date-parts":[[2013,4,16]],"date-time":"2013-04-16T11:40:48Z","timestamp":1366112448000},"page":"321-332","source":"Crossref","is-referenced-by-count":35,"title":["Prion Disease: A Tale of Folds and Strains"],"prefix":"10.1111","volume":"23","author":[{"given":"Hans","family":"Kretzschmar","sequence":"first","affiliation":[{"name":"Institut f\u00fcr Neuropathologie  M\u00fcnchen"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f6rg","family":"Tatzelt","sequence":"additional","affiliation":[{"name":"Neurobiochemistry Adolf\u2010Butenandt\u2010Institute Ludwig\u2010Maximilians\u2010University Munich  Munich 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