Abstract
Mammalian transmissible spongiform encephalopathy (prion) and amyloid diseases seem to involve the self-propagation of abnormal fibrillar or sub-fibrillar protein aggregates. Similar processes explain protein-mediated inheritance by yeast prions. Indeed, yeast prions are more surely mediated solely by aberrant protein aggregates than are their mammalian namesakes. Tantalizing parallels make yeast prions attractive models of mammalian protein-folding diseases.
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