期刊
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE
卷 8, 期 5, 页码 -出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/cshperspect.a023507
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资金
- Canadian Institutes of Health Research
- Alzheimer Society Canada
- National Institutes of Health [AG002132, AG031220]
- Dana Foundation
- Glenn Foundation
- Sherman Fairchild Foundation
Alzheimer's disease (AD) is the most common neurodegenerative disease in humans and will pose a considerable challenge to healthcare systems in the coming years. Aggregation of the beta-amyloid (A beta) peptide within the brain is thought to be an initiating event in AD pathogenesis. Many recent studies in transgenic mice have provided evidence that A beta aggregates become self-propagating during disease, leading to a cascade of protein aggregation in the brain, which may underlie the progressive nature of AD. The ability to self-propagate and the existence of distinct strains reveals that A beta aggregates exhibit many properties indistinguishable from those of prions composed of PrPSc proteins. Here, we review the evidence that A beta can become a prion during disease and discuss how A beta prions may be important for understanding the pathobiology of AD.
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