Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism
Prions are considered the best example to prove that the biological information can be transferred protein to protein through a conformational change. The term “prion-like” is used to describe molecular mechanisms that share similarities with the mammalian prion protein self-perpetuating aggregation...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2013/583498 |
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| author | Natalia Fernández-Borges Hasier Eraña Saioa R. Elezgarai Chafik Harrathi Mayela Gayosso Joaquín Castilla |
| author_facet | Natalia Fernández-Borges Hasier Eraña Saioa R. Elezgarai Chafik Harrathi Mayela Gayosso Joaquín Castilla |
| author_sort | Natalia Fernández-Borges |
| collection | DOAJ |
| description | Prions are considered the best example to prove that the biological information can be transferred protein to protein through a conformational change. The term “prion-like” is used to describe molecular mechanisms that share similarities with the mammalian prion protein self-perpetuating aggregation and spreading characteristics. Since prions are presumably composed only of protein and are infectious, the more similar the mechanisms that occur in the different neurodegenerative diseases, the more these processes will resemble an infection. In vitro and in vivo experiments carried out during the last decade in different neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's diseases (PD), and amyotrophic lateral sclerosis (ALS) have shown a convergence toward a unique mechanism of misfolded protein propagation. In spite of the term “infection” that could be used to explain the mechanism governing the diversity of the pathological processes, other concepts as “seeding” or “de novo induction” are being used to describe the in vivo propagation and transmissibility of misfolded proteins. The current studies are demanding an extended definition of “disease-causing agents” to include those already accepted as well as other misfolded proteins. In this new scenario, “seeding” would be a type of mechanism by which an infectious agent can be transmitted but should not be used to define a whole “infection” process. |
| format | Article |
| id | doaj-art-06de1e13d78f480d8ae29e3221cfefd6 |
| institution | OA Journals |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-06de1e13d78f480d8ae29e3221cfefd62025-08-20T02:02:50ZengWileyInternational Journal of Cell Biology1687-88761687-88842013-01-01201310.1155/2013/583498583498Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like MechanismNatalia Fernández-Borges0Hasier Eraña1Saioa R. Elezgarai2Chafik Harrathi3Mayela Gayosso4Joaquín Castilla5CIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainCIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainCIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainCIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainCIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainCIC bioGUNE, Parque Tecnológico de Bizkaia, Derio, 48160 Bizkaia, SpainPrions are considered the best example to prove that the biological information can be transferred protein to protein through a conformational change. The term “prion-like” is used to describe molecular mechanisms that share similarities with the mammalian prion protein self-perpetuating aggregation and spreading characteristics. Since prions are presumably composed only of protein and are infectious, the more similar the mechanisms that occur in the different neurodegenerative diseases, the more these processes will resemble an infection. In vitro and in vivo experiments carried out during the last decade in different neurodegenerative disorders such as Alzheimer's disease (AD), Parkinson's diseases (PD), and amyotrophic lateral sclerosis (ALS) have shown a convergence toward a unique mechanism of misfolded protein propagation. In spite of the term “infection” that could be used to explain the mechanism governing the diversity of the pathological processes, other concepts as “seeding” or “de novo induction” are being used to describe the in vivo propagation and transmissibility of misfolded proteins. The current studies are demanding an extended definition of “disease-causing agents” to include those already accepted as well as other misfolded proteins. In this new scenario, “seeding” would be a type of mechanism by which an infectious agent can be transmitted but should not be used to define a whole “infection” process.http://dx.doi.org/10.1155/2013/583498 |
| spellingShingle | Natalia Fernández-Borges Hasier Eraña Saioa R. Elezgarai Chafik Harrathi Mayela Gayosso Joaquín Castilla Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism International Journal of Cell Biology |
| title | Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism |
| title_full | Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism |
| title_fullStr | Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism |
| title_full_unstemmed | Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism |
| title_short | Infectivity versus Seeding in Neurodegenerative Diseases Sharing a Prion-Like Mechanism |
| title_sort | infectivity versus seeding in neurodegenerative diseases sharing a prion like mechanism |
| url | http://dx.doi.org/10.1155/2013/583498 |
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