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- W2002060061 abstract "Creutzfeldt-Jakob disease (CJD), particularly its predominant sporadic form (sCJD), is the prototype of human prion diseases—a small family of rare, fatal, and untreatable neurodegenerative disorders affecting about 1–2 persons per million per year.1 CJD is linked to pathologic alteration of an endogenous cellular protein, the prion protein (PrP). However, in contrast to other neurodegenerative dementias involving proteinopathy, prion diseases are transmissible between individuals by an infection-like process, in which disease-associated PrP (PrPD) can “replicate” exponentially by templating the misfolding of normal cellular PrP (PrPC). This discovery inspired the term “prion” in order to denote the implicated proteinaceous infectious particle (Greek suffix “-on”).2 Prions are notoriously difficult to remove and/or inactivate with routine disinfection methods, and evidence of accidental CJD transmission in the health care setting has been documented.3,4 Thus, in suspected sCJD, the importance of timely, accurate diagnosis is accentuated by the need to manage the risk of secondary exposure to prion infectivity, particularly through reuse of surgical or other instruments.5" @default.
- W2002060061 created "2016-06-24" @default.
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- W2002060061 date "2015-01-29" @default.
- W2002060061 modified "2023-09-23" @default.
- W2002060061 title "Creutzfeldt-Jakob disease" @default.
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- W2002060061 doi "https://doi.org/10.1212/cpj.0000000000000103" @default.
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