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The discovery of misfolded prions as an infectious agent

INTRODUCTION The Nobel Prize in Physiology or Medicine for 1976 was coawarded to Daniel Carleton Gajdusek (1923–2008) for the discovery of a new type of infectious agent (as well as to Baruch Blumberg for discoveries in virology). In 1997, the Prize was awarded to Stanley Prusiner (1942-) for demonstrating that this infectious agent consists of a misfolded prion protein, which Prusiner has designated as PrP. These two Nobel laureates paved the way for a new field of neurobiology with important implications for clinical and veterinary medicine. The fascinating story of their discoveries began in 1954 when the Icelander Bjorn Sigurdsson introduced the concept of ‘slow infections’ (1) after the studies of the diseases ‘maedi’ and ‘rida’ that were prevalent in Islandic sheep. In 1957, Sigurdsson and coworkers suggested that the ‘rida’ may be similar to a fatal coatagius encephalitis and that was characterized by trembling ataxia, dementia and spongioform encephalopathy (2), and which disease they considered to be identical with ‘scrapie’, as described 1950 by Wilson et al. (3). Following the publication of his report, others began to question whether the neurodegenerative disease kuru, which was seen in people from the mountainous area of New Guinea, had a similar aetiology to scrapie (4).