Prions and Prion-Like Pathogens in Neurodegenerative Disorders
Prions are unique elements in biology, being able to transmit biological information from one organism to another in the absence of nucleic acids. They have been identified as self-replicating proteinaceous agents responsible for the onset of rare and fatal neurodegenerative disorders—known as tran...
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doaj-e21b4adf6a6c404985f4d2ae00761cc82020-11-24T22:28:52ZengMDPI AGPathogens2076-08172014-02-013114916310.3390/pathogens3010149pathogens3010149Prions and Prion-Like Pathogens in Neurodegenerative DisordersCaterina Peggion0Maria Catia Sorgato1Alessandro Bertoli2Department of Biomedical Sciences, University of Padova, Viale G. Colombo 3, Padova 35131, ItalyDepartment of Biomedical Sciences, University of Padova, Viale G. Colombo 3, Padova 35131, ItalyDepartment of Biomedical Sciences, University of Padova, Viale G. Colombo 3, Padova 35131, ItalyPrions are unique elements in biology, being able to transmit biological information from one organism to another in the absence of nucleic acids. They have been identified as self-replicating proteinaceous agents responsible for the onset of rare and fatal neurodegenerative disorders—known as transmissible spongiform encephalopathies, or prion diseases—which affect humans and other animal species. More recently, it has been proposed that other proteins associated with common neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, can self-replicate like prions, thus sustaining the spread of neurotoxic entities throughout the nervous system. Here, we review findings that have contributed to expand the prion concept, and discuss if the involved toxic species can be considered bona fide prions, including the capacity to infect other organisms, or whether these pathogenic aggregates share with prions only the capability to self-replicate.http://www.mdpi.com/2076-0817/3/1/149prionprion-likePrPneurodegenerationamyloid-βtauα-synucleinAlzheimer’s diseaseParkinson’s disease |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Caterina Peggion Maria Catia Sorgato Alessandro Bertoli |
spellingShingle |
Caterina Peggion Maria Catia Sorgato Alessandro Bertoli Prions and Prion-Like Pathogens in Neurodegenerative Disorders Pathogens prion prion-like PrP neurodegeneration amyloid-β tau α-synuclein Alzheimer’s disease Parkinson’s disease |
author_facet |
Caterina Peggion Maria Catia Sorgato Alessandro Bertoli |
author_sort |
Caterina Peggion |
title |
Prions and Prion-Like Pathogens in Neurodegenerative Disorders |
title_short |
Prions and Prion-Like Pathogens in Neurodegenerative Disorders |
title_full |
Prions and Prion-Like Pathogens in Neurodegenerative Disorders |
title_fullStr |
Prions and Prion-Like Pathogens in Neurodegenerative Disorders |
title_full_unstemmed |
Prions and Prion-Like Pathogens in Neurodegenerative Disorders |
title_sort |
prions and prion-like pathogens in neurodegenerative disorders |
publisher |
MDPI AG |
series |
Pathogens |
issn |
2076-0817 |
publishDate |
2014-02-01 |
description |
Prions are unique elements in biology, being able to transmit biological information from one organism to another in the absence of nucleic acids. They have been identified as self-replicating proteinaceous agents responsible for the onset of rare and fatal neurodegenerative disorders—known as transmissible spongiform encephalopathies, or prion diseases—which affect humans and other animal species. More recently, it has been proposed that other proteins associated with common neurodegenerative disorders, such as Alzheimer’s and Parkinson’s disease, can self-replicate like prions, thus sustaining the spread of neurotoxic entities throughout the nervous system. Here, we review findings that have contributed to expand the prion concept, and discuss if the involved toxic species can be considered bona fide prions, including the capacity to infect other organisms, or whether these pathogenic aggregates share with prions only the capability to self-replicate. |
topic |
prion prion-like PrP neurodegeneration amyloid-β tau α-synuclein Alzheimer’s disease Parkinson’s disease |
url |
http://www.mdpi.com/2076-0817/3/1/149 |
work_keys_str_mv |
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