Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10956511 | Molecular and Cellular Neuroscience | 2015 | 9 Pages |
Abstract
Prion diseases are fatal neurodegenerative disorders. Pathology is closely linked to the misfolding of native cellular PrPC into the disease-associated form PrPSc that accumulates in the brain as disease progresses. Although treatments have yet to be developed, strategies aimed at stimulating the degradation of PrPSc have shown efficacy in experimental models of prion disease. Here, we describe the cellular pathways that mediate PrPSc degradation and review possible targets for therapeutic intervention. This article is part of a Special Issue entitled 'Neuronal Protein'.
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Authors
Rob Goold, Chris McKinnon, Sarah J. Tabrizi,