Oxidative damage to nucleic acids in human prion disease

Marin Guentchev, Sandra L. Siedlak, Christa Jarius, Fabrizio Tagliavini, Rudy J. Castellani, George Perry, Mark A. Smith, Herbert Budka*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

72 Scopus citations


Recently, several studies proposed a physiological role for the cellular prion protein (PrPc) in defense against oxidative stress. Since the pathogenesis of prion disease necessarily involves a disturbance of PrPc homeostasis, we hypothesized that such diseases would be associated with concomitant disturbances in oxidative balance. In support of such a notion, in this study we show increased oxidative damage to nucleic acids in affected brains of patients with Creutzfeldt-Jakob disease. These data suggest that damage by free radicals is a likely cause for neurodegeneration in human prion disease, and antioxidants are a potential therapy for these disorders. Further, our data support the hypothesis that loss of the anti-oxidant function of PrPc plays a key role in the pathogenesis of these disorders.

Original languageEnglish (US)
Pages (from-to)275-281
Number of pages7
JournalNeurobiology of Disease
Issue number3
StatePublished - 2002

ASJC Scopus subject areas

  • Neurology


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