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Redox Imbalance and Viral Infections in Neurodegenerative Diseases

Reactive oxygen species (ROS) are essential molecules for many physiological functions and act as second messengers in a large variety of tissues. An imbalance in the production and elimination of ROS is associated with human diseases including neurodegenerative disorders. In the last years the noti...

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Autores principales: Limongi, Dolores, Baldelli, Sara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826696/
https://www.ncbi.nlm.nih.gov/pubmed/27110325
http://dx.doi.org/10.1155/2016/6547248
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author Limongi, Dolores
Baldelli, Sara
author_facet Limongi, Dolores
Baldelli, Sara
author_sort Limongi, Dolores
collection PubMed
description Reactive oxygen species (ROS) are essential molecules for many physiological functions and act as second messengers in a large variety of tissues. An imbalance in the production and elimination of ROS is associated with human diseases including neurodegenerative disorders. In the last years the notion that neurodegenerative diseases are accompanied by chronic viral infections, which may result in an increase of neurodegenerative diseases progression, emerged. It is known in literature that enhanced viral infection risk, observed during neurodegeneration, is partly due to the increase of ROS accumulation in brain cells. However, the molecular mechanisms of viral infection, occurring during the progression of neurodegeneration, remain unclear. In this review, we discuss the recent knowledge regarding the role of influenza, herpes simplex virus type-1, and retroviruses infection in ROS/RNS-mediated Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS).
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spelling pubmed-48266962016-04-24 Redox Imbalance and Viral Infections in Neurodegenerative Diseases Limongi, Dolores Baldelli, Sara Oxid Med Cell Longev Review Article Reactive oxygen species (ROS) are essential molecules for many physiological functions and act as second messengers in a large variety of tissues. An imbalance in the production and elimination of ROS is associated with human diseases including neurodegenerative disorders. In the last years the notion that neurodegenerative diseases are accompanied by chronic viral infections, which may result in an increase of neurodegenerative diseases progression, emerged. It is known in literature that enhanced viral infection risk, observed during neurodegeneration, is partly due to the increase of ROS accumulation in brain cells. However, the molecular mechanisms of viral infection, occurring during the progression of neurodegeneration, remain unclear. In this review, we discuss the recent knowledge regarding the role of influenza, herpes simplex virus type-1, and retroviruses infection in ROS/RNS-mediated Parkinson's disease (PD), Alzheimer's disease (AD), and amyotrophic lateral sclerosis (ALS). Hindawi Publishing Corporation 2016 2016-03-27 /pmc/articles/PMC4826696/ /pubmed/27110325 http://dx.doi.org/10.1155/2016/6547248 Text en Copyright © 2016 D. Limongi and S. Baldelli. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Limongi, Dolores
Baldelli, Sara
Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title_full Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title_fullStr Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title_full_unstemmed Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title_short Redox Imbalance and Viral Infections in Neurodegenerative Diseases
title_sort redox imbalance and viral infections in neurodegenerative diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4826696/
https://www.ncbi.nlm.nih.gov/pubmed/27110325
http://dx.doi.org/10.1155/2016/6547248
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