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How an Infection of Sheep Revealed Prion Mechanisms in Alzheimer's Disease and Other Neurodegenerative Disorders.
- Source :
-
International journal of molecular sciences [Int J Mol Sci] 2021 May 04; Vol. 22 (9). Date of Electronic Publication: 2021 May 04. - Publication Year :
- 2021
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Abstract
- Although it is not yet universally accepted that all neurodegenerative diseases (NDs) are prion disorders, there is little disagreement that Alzheimer's disease (AD), Parkinson's disease, frontotemporal dementia (FTD), and other NDs are a consequence of protein misfolding, aggregation, and spread. This widely accepted perspective arose from the prion hypothesis, which resulted from investigations on scrapie, a common transmissible disease of sheep and goats. The prion hypothesis argued that the causative infectious agent of scrapie was a novel proteinaceous pathogen devoid of functional nucleic acids and distinct from viruses, viroids, and bacteria. At the time, it seemed impossible that an infectious agent like the one causing scrapie could replicate and exist as diverse microbiological strains without nucleic acids. However, aggregates of a misfolded host-encoded protein, designated the prion protein (PrP), were shown to be the cause of scrapie as well as Creutzfeldt-Jakob disease (CJD) and Gerstmann-Sträussler-Scheinker syndrome (GSS), which are similar NDs in humans. This review discusses historical research on diseases caused by PrP misfolding, emphasizing principles of pathogenesis that were later found to be core features of other NDs. For example, the discovery that familial prion diseases can be caused by mutations in PrP was important for understanding prion replication and disease susceptibility not only for rare PrP diseases but also for far more common NDs involving other proteins. We compare diseases caused by misfolding and aggregation of APP-derived Aβ peptides, tau, and α-synuclein with PrP prion disorders and argue for the classification of NDs caused by misfolding of these proteins as prion diseases. Deciphering the molecular pathogenesis of NDs as prion-mediated has provided new approaches for finding therapies for these intractable, invariably fatal disorders and has revolutionized the field.
- Subjects :
- Alzheimer Disease etiology
Alzheimer Disease metabolism
Alzheimer Disease pathology
Amyloid beta-Peptides chemistry
Amyloid beta-Peptides metabolism
Animals
Creutzfeldt-Jakob Syndrome etiology
Creutzfeldt-Jakob Syndrome genetics
Creutzfeldt-Jakob Syndrome metabolism
Creutzfeldt-Jakob Syndrome pathology
Frontotemporal Dementia etiology
Frontotemporal Dementia genetics
Frontotemporal Dementia metabolism
Frontotemporal Dementia pathology
Gene Expression
Gerstmann-Straussler-Scheinker Disease etiology
Gerstmann-Straussler-Scheinker Disease genetics
Gerstmann-Straussler-Scheinker Disease metabolism
Gerstmann-Straussler-Scheinker Disease pathology
Humans
Mice
Mutation
Parkinson Disease etiology
Parkinson Disease genetics
Parkinson Disease metabolism
Parkinson Disease pathology
Prion Proteins chemistry
Prion Proteins metabolism
Prions
Protein Folding
Scrapie etiology
Scrapie metabolism
Scrapie pathology
Sheep
alpha-Synuclein chemistry
alpha-Synuclein metabolism
tau Proteins chemistry
tau Proteins metabolism
Alzheimer Disease genetics
Amyloid beta-Peptides genetics
Prion Proteins genetics
Scrapie genetics
alpha-Synuclein genetics
tau Proteins genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1422-0067
- Volume :
- 22
- Issue :
- 9
- Database :
- MEDLINE
- Journal :
- International journal of molecular sciences
- Publication Type :
- Academic Journal
- Accession number :
- 34064393
- Full Text :
- https://doi.org/10.3390/ijms22094861