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Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases

There is a growing body of evidence that prionoid protein behaviors are a core element of neurodegenerative diseases (NDs) that afflict humans. Common elements in pathogenesis, pathological effects and protein-level behaviors exist between Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntingt...

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Autores principales: Wells, Cameron, Brennan, Samuel E., Keon, Matt, Saksena, Nitin K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861308/
https://www.ncbi.nlm.nih.gov/pubmed/31780895
http://dx.doi.org/10.3389/fnmol.2019.00271
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author Wells, Cameron
Brennan, Samuel E.
Keon, Matt
Saksena, Nitin K.
author_facet Wells, Cameron
Brennan, Samuel E.
Keon, Matt
Saksena, Nitin K.
author_sort Wells, Cameron
collection PubMed
description There is a growing body of evidence that prionoid protein behaviors are a core element of neurodegenerative diseases (NDs) that afflict humans. Common elements in pathogenesis, pathological effects and protein-level behaviors exist between Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’s Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). These extend beyond the affected neurons to glial cells and processes. This results in a complicated system of disease progression, which often takes advantage of protective processes to promote the propagation of pathological protein aggregates. This review article provides a current snapshot of knowledge on these proteins and their intrinsic role in the pathogenesis and disease progression seen across NDs.
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spelling pubmed-68613082019-11-28 Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases Wells, Cameron Brennan, Samuel E. Keon, Matt Saksena, Nitin K. Front Mol Neurosci Neuroscience There is a growing body of evidence that prionoid protein behaviors are a core element of neurodegenerative diseases (NDs) that afflict humans. Common elements in pathogenesis, pathological effects and protein-level behaviors exist between Alzheimer’s Disease (AD), Parkinson’s Disease (PD), Huntington’s Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). These extend beyond the affected neurons to glial cells and processes. This results in a complicated system of disease progression, which often takes advantage of protective processes to promote the propagation of pathological protein aggregates. This review article provides a current snapshot of knowledge on these proteins and their intrinsic role in the pathogenesis and disease progression seen across NDs. Frontiers Media S.A. 2019-11-12 /pmc/articles/PMC6861308/ /pubmed/31780895 http://dx.doi.org/10.3389/fnmol.2019.00271 Text en Copyright © 2019 Wells, Brennan, Keon and Saksena. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Wells, Cameron
Brennan, Samuel E.
Keon, Matt
Saksena, Nitin K.
Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title_full Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title_fullStr Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title_full_unstemmed Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title_short Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases
title_sort prionoid proteins in the pathogenesis of neurodegenerative diseases
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6861308/
https://www.ncbi.nlm.nih.gov/pubmed/31780895
http://dx.doi.org/10.3389/fnmol.2019.00271
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