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Oxidative damage to nucleic acids in human prion disease
Marin Guentchev1, Sandra L Siedlak, Christa Jarius
1Institute of Neurology, University of Vienna, Austrian Reference Center for Human Prion Disease (ORPE).
Neurobiology of Disease
|April 13, 2002
Summary
Oxidative damage to nucleic acids is increased in Creutzfeldt-Jakob disease brains, suggesting free radical damage contributes to neurodegeneration. Loss of the cellular prion protein
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Cellular prion protein (PrP(c)) may play a role in combating oxidative stress.
- Prion disease pathogenesis involves disruption of PrP(c) homeostasis.
- Oxidative balance disturbances are hypothesized to accompany prion diseases.
Purpose of the Study:
- To investigate the association between prion diseases and oxidative balance disturbances.
- To determine if oxidative damage occurs in the brains of Creutzfeldt-Jakob disease patients.
- To explore the role of PrP(c) antioxidant function in prion disease pathogenesis.
Main Methods:
- Analysis of oxidative damage to nucleic acids in affected brain tissue from Creutzfeldt-Jakob disease patients.
- Comparison of oxidative damage levels with control brain tissue (implied).
Main Results:
- Increased oxidative damage to nucleic acids was observed in the brains of Creutzfeldt-Jakob disease patients.
- These findings support the hypothesis of concomitant disturbances in oxidative balance during prion disease.
Conclusions:
- Free radical damage is a likely contributor to neurodegeneration in human prion diseases.
- Antioxidants represent a potential therapeutic strategy for prion disorders.
- The loss of PrP(c)'s antioxidant function is implicated as a key factor in prion disease pathogenesis.