Mice devoid of prion protein have cognitive deficits that are rescued by reconstitution of PrP in neurons

Prion protein (PrPC) is a constituent of most normal mammalian cells and plays an essential role in the pathogenesis of transmissible spongiform encephalopathies (TSE). However, the normal cellular function of PrPC remains unclear. Here, we document that mice with a selective deletion of PrPC exhibi...

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Bibliographic Details
Main Authors: José R. Criado, Manuel Sánchez-Alavez, Bruno Conti, Jeannie L. Giacchino, Derek N. Wills, Steven J. Henriksen, Richard Race, Jean C. Manson, Bruce Chesebro, Michael B.A. Oldstone
Format: Article
Language:English
Published: Elsevier 2005-06-01
Series:Neurobiology of Disease
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996105000070