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

Research output: Contribution to journalArticle

Abstract

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
Pages (from-to)275-281
Number of pages7
JournalNeurobiology of Disease
Volume9
Issue number3
DOIs
Publication statusPublished - 2002

ASJC Scopus subject areas

  • Neurology

Fingerprint Dive into the research topics of 'Oxidative damage to nucleic acids in human prion disease'. Together they form a unique fingerprint.

  • Cite this

    Guentchev, M., Siedlak, S. L., Jarius, C., Tagliavini, F., Castellani, R. J., Perry, G., Smith, M. A., & Budka, H. (2002). Oxidative damage to nucleic acids in human prion disease. Neurobiology of Disease, 9(3), 275-281. https://doi.org/10.1006/nbdi.2002.0477