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The prion-like propagation hypothesis in Alzheimer's and Parkinson's disease.
Curr Opin Neurol. 2019 04; 32(2):266-271.CO

Abstract

PURPOSE OF REVIEW

This study, taking the example of Alzheimer's and Parkinson's diseases, presents the experimental and human data that support the hypothesis that Aβ, tau, and α-synuclein may seed and propagate the pathology and consider the potential clinical consequences.

RECENT FINDINGS

Aβ aggregates transmit Aβ pathology to experimental animals. Interhuman transmission of Aβ pathology has also been observed in iatrogenic Creutzfeldt-Jakob disease, or after dural graft. Tau aggregates also transmit the pathology to mice when injected in the brain and propagates along neuronal pathways. Evidence of interhuman transmission is weak. Finally α-synuclein aggregates, when injected in specific areas of the brain may recapitulate Lewy pathology of Parkinson's disease but there is currently no hint of human to human transmission.

SUMMARY

Since the first evidence that at least Aβ pathology of Alzheimer's disease could be transmitted to the animal, data have accumulated indicating that misfolded proteins characteristic of neurodegenerative diseases may seed and propagate pathology in a prion-like manner. The term propagon has been proposed to describe those proteins that act as prions at different levels. Taking the example of Alzheimer's and Parkinson's diseases, the experimental and human data supporting the hypothesis that Aβ, tau, and α-synuclein are indeed propagons are presented with their clinical consequences.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Duyckaerts C
Sorbonne Université, Assistance Publique des Hôpitaux de Paris.
Clavaguera F
Equipe Alzheimer-Prion, Institut du Cerveau et de la Moelle (ICM), Paris, France.
Potier MC
Equipe Alzheimer-Prion, Institut du Cerveau et de la Moelle (ICM), Paris, France.

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesHumansParkinson DiseasePrion DiseasesPrionsalpha-Synucleintau Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

30724769

Citation

Duyckaerts, Charles, et al. "The Prion-like Propagation Hypothesis in Alzheimer's and Parkinson's Disease." Current Opinion in Neurology, vol. 32, no. 2, 2019, pp. 266-271.
Duyckaerts C, Clavaguera F, Potier MC. The prion-like propagation hypothesis in Alzheimer's and Parkinson's disease. Curr Opin Neurol. 2019;32(2):266-271.
Duyckaerts, C., Clavaguera, F., & Potier, M. C. (2019). The prion-like propagation hypothesis in Alzheimer's and Parkinson's disease. Current Opinion in Neurology, 32(2), 266-271. https://doi.org/10.1097/WCO.0000000000000672
Duyckaerts C, Clavaguera F, Potier MC. The Prion-like Propagation Hypothesis in Alzheimer's and Parkinson's Disease. Curr Opin Neurol. 2019;32(2):266-271. PubMed PMID: 30724769.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The prion-like propagation hypothesis in Alzheimer's and Parkinson's disease. AU - Duyckaerts,Charles, AU - Clavaguera,Florence, AU - Potier,Marie-Claude, PY - 2019/2/7/pubmed PY - 2020/1/11/medline PY - 2019/2/7/entrez SP - 266 EP - 271 JF - Current opinion in neurology JO - Curr Opin Neurol VL - 32 IS - 2 N2 - PURPOSE OF REVIEW: This study, taking the example of Alzheimer's and Parkinson's diseases, presents the experimental and human data that support the hypothesis that Aβ, tau, and α-synuclein may seed and propagate the pathology and consider the potential clinical consequences. RECENT FINDINGS: Aβ aggregates transmit Aβ pathology to experimental animals. Interhuman transmission of Aβ pathology has also been observed in iatrogenic Creutzfeldt-Jakob disease, or after dural graft. Tau aggregates also transmit the pathology to mice when injected in the brain and propagates along neuronal pathways. Evidence of interhuman transmission is weak. Finally α-synuclein aggregates, when injected in specific areas of the brain may recapitulate Lewy pathology of Parkinson's disease but there is currently no hint of human to human transmission. SUMMARY: Since the first evidence that at least Aβ pathology of Alzheimer's disease could be transmitted to the animal, data have accumulated indicating that misfolded proteins characteristic of neurodegenerative diseases may seed and propagate pathology in a prion-like manner. The term propagon has been proposed to describe those proteins that act as prions at different levels. Taking the example of Alzheimer's and Parkinson's diseases, the experimental and human data supporting the hypothesis that Aβ, tau, and α-synuclein are indeed propagons are presented with their clinical consequences. SN - 1473-6551 UR - https://www.unboundmedicine.com/medline/citation/30724769/The_prion_like_propagation_hypothesis_in_Alzheimer's_and_Parkinson's_disease_ DB - PRIME DP - Unbound Medicine ER -