Abstract
Alzheimer's disease is a major neurodegenerative disease of the brain, the incidence of which increases dramatically in old age. Currently, no drugs are available to halt or slow the progression of this disease, which poses an ever-expanding burden on health services, families and society. The prion protein has become infamous owing to its role as the causative agent of the transmissible spongiform encephalopathies such as Creutzfeldt-Jakob disease in humans. However, our view of the prion protein as an unwanted, harmful entity has been challenged recently. New data indicate that the normal cellular form of the prion protein might have a crucial role in suppressing the production of the amyloid-beta peptide, the neurotoxic molecule involved in the pathogenesis of Alzheimer's disease.
Original language | English |
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Pages (from-to) | 151-155 |
Number of pages | 5 |
Journal | Trends Biochem Sci |
Volume | 33 |
DOIs | |
Publication status | Published - 2008 |
Research Beacons, Institutes and Platforms
- Dementia@Manchester