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Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases

DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eu-karyotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombina-tion, DNA replication and transcription. Deregulation of DSBs has been...

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Autores principales: Zhu, Ling-Shuang, Wang, Ding-Qi, Cui, Ke, Liu, Dan, Zhu, Ling-Qiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Science Publishers 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057204/
https://www.ncbi.nlm.nih.gov/pubmed/31362659
http://dx.doi.org/10.2174/1570159X17666190726115623
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author Zhu, Ling-Shuang
Wang, Ding-Qi
Cui, Ke
Liu, Dan
Zhu, Ling-Qiang
author_facet Zhu, Ling-Shuang
Wang, Ding-Qi
Cui, Ke
Liu, Dan
Zhu, Ling-Qiang
author_sort Zhu, Ling-Shuang
collection PubMed
description DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eu-karyotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombina-tion, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative dis-orders including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) and ataxia tel-angiectasia (A-T).
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spelling pubmed-70572042020-06-01 Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases Zhu, Ling-Shuang Wang, Ding-Qi Cui, Ke Liu, Dan Zhu, Ling-Qiang Curr Neuropharmacol Article DNA double-strand breaks (DSBs) are common events that were recognized as one of the most toxic lesions in eu-karyotic cells. DSBs are widely involved in many physiological processes such as V(D)J recombination, meiotic recombina-tion, DNA replication and transcription. Deregulation of DSBs has been reported in multiple diseases in human beings, such as the neurodegenerative diseases, with which the underlying mechanisms are needed to be illustrated. Here, we reviewed the recent insights into the dysfunction of DSB formation and repair, contributing to the pathogenesis of neurodegenerative dis-orders including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD) and ataxia tel-angiectasia (A-T). Bentham Science Publishers 2019-12 2019-12 /pmc/articles/PMC7057204/ /pubmed/31362659 http://dx.doi.org/10.2174/1570159X17666190726115623 Text en © 2019 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) (https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.
spellingShingle Article
Zhu, Ling-Shuang
Wang, Ding-Qi
Cui, Ke
Liu, Dan
Zhu, Ling-Qiang
Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title_full Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title_fullStr Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title_full_unstemmed Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title_short Emerging Perspectives on DNA Double-strand Breaks in Neurodegenerative Diseases
title_sort emerging perspectives on dna double-strand breaks in neurodegenerative diseases
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057204/
https://www.ncbi.nlm.nih.gov/pubmed/31362659
http://dx.doi.org/10.2174/1570159X17666190726115623
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