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Association Between Autophagy and Neurodegenerative Diseases
Autophagy is a phylogenetically conserved mechanism that controls the degradation of subcellular constituents, including misfolded proteins, and damaged organelles. The progression of many neurodegenerative diseases is thought to be driven by the aggregation of misfolded proteins; therefore, autopha...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5972210/ https://www.ncbi.nlm.nih.gov/pubmed/29872373 http://dx.doi.org/10.3389/fnins.2018.00255 |
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author | Fujikake, Nobuhiro Shin, Minkyoung Shimizu, Shigeomi |
author_facet | Fujikake, Nobuhiro Shin, Minkyoung Shimizu, Shigeomi |
author_sort | Fujikake, Nobuhiro |
collection | PubMed |
description | Autophagy is a phylogenetically conserved mechanism that controls the degradation of subcellular constituents, including misfolded proteins, and damaged organelles. The progression of many neurodegenerative diseases is thought to be driven by the aggregation of misfolded proteins; therefore, autophagic activity is thought to affect disease severity to some extent. In some neurodegenerative diseases, the suppression of autophagic activity accelerates disease progression. Given that the induction of autophagy can potentially mitigate disease severity, various autophagy-inducing compounds have been developed and their efficacy has been evaluated in several rodent models of neurodegenerative diseases. |
format | Online Article Text |
id | pubmed-5972210 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-59722102018-06-05 Association Between Autophagy and Neurodegenerative Diseases Fujikake, Nobuhiro Shin, Minkyoung Shimizu, Shigeomi Front Neurosci Neuroscience Autophagy is a phylogenetically conserved mechanism that controls the degradation of subcellular constituents, including misfolded proteins, and damaged organelles. The progression of many neurodegenerative diseases is thought to be driven by the aggregation of misfolded proteins; therefore, autophagic activity is thought to affect disease severity to some extent. In some neurodegenerative diseases, the suppression of autophagic activity accelerates disease progression. Given that the induction of autophagy can potentially mitigate disease severity, various autophagy-inducing compounds have been developed and their efficacy has been evaluated in several rodent models of neurodegenerative diseases. Frontiers Media S.A. 2018-05-22 /pmc/articles/PMC5972210/ /pubmed/29872373 http://dx.doi.org/10.3389/fnins.2018.00255 Text en Copyright © 2018 Fujikake, Shin and Shimizu. 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 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 Fujikake, Nobuhiro Shin, Minkyoung Shimizu, Shigeomi Association Between Autophagy and Neurodegenerative Diseases |
title | Association Between Autophagy and Neurodegenerative Diseases |
title_full | Association Between Autophagy and Neurodegenerative Diseases |
title_fullStr | Association Between Autophagy and Neurodegenerative Diseases |
title_full_unstemmed | Association Between Autophagy and Neurodegenerative Diseases |
title_short | Association Between Autophagy and Neurodegenerative Diseases |
title_sort | association between autophagy and neurodegenerative diseases |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5972210/ https://www.ncbi.nlm.nih.gov/pubmed/29872373 http://dx.doi.org/10.3389/fnins.2018.00255 |
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