期刊
ANNUAL REVIEW OF NEUROSCIENCE, VOL 38
卷 38, 期 -, 页码 87-103出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-neuro-071714-033828
关键词
Alzheimer's disease; amyloid; cell-to-cell spreading; disease progression; Parkinson's disease; tau; synuclein; proteopathy; transmission; prion
资金
- Competence Network on Degenerative Dementias [BMBF-01GI0705]
- ALZKULT [BMBF-031A198A]
- US National Institutes of Health [AG040589, RR000165, OD11132, AG025688]
- CART Foundation
- MetLife Foundation
- NATIONAL CENTER FOR RESEARCH RESOURCES [P51RR000165] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R21AG040589, P50AG025688] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [P51OD011132] Funding Source: NIH RePORTER
The prion paradigm has emerged as a unifying molecular principle for the pathogenesis of many age-related neurodegenerative diseases. This paradigm holds that a fundamental cause of specific disorders is the misfolding and seeded aggregation of certain proteins. The concept arose from the discovery that devastating brain diseases called spongiform encephalopathies are transmissible to new hosts by agents consisting solely of a misfolded protein, now known as the prion protein. Accordingly, prion was defined as a proteinaceous infectious particle. As the concept has expanded to include other diseases, many of which are not infectious by any conventional definition, the designation of prions as infectious agents has become problematic. We propose to define prions as proteinaceous nucleating particles to highlight the molecular action of the agents, lessen unwarranted apprehension about the transmissibility of noninfectious proteopathies, and promote the wider acceptance of this revolutionary paradigm by the biomedical community.
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