Abstract
The relation among Creuztfeldt-Jakob disease (CJD), its recently described new variant (vCJD), and bovine spongiform encephalopathy (BSE) has been the focus of much biologic and epidemiologic interest since vCJD was first reported three years ago. Although the mechanisms through which prions cause neurologic disease remain unclear, current understanding focuses on the alteration of a normal cellular protein (PrPC) into an abnormal isoform (PrPSc). With this change comes the …
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