DNA Damage Repair in Huntington's Disease and Other Neurodegenerative Diseases.
Ataxia telangiectasia-mutated (ATM)
DNA repair
Huntington’s disease
Oxidative stress
Poly ADP-ribose polymerase (PARP)
Spinocerebellar ataxia
Journal
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics
ISSN: 1878-7479
Titre abrégé: Neurotherapeutics
Pays: United States
ID NLM: 101290381
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
pubmed:
1
8
2019
medline:
25
8
2020
entrez:
1
8
2019
Statut:
ppublish
Résumé
Recent genome-wide association studies of Huntington's disease (HD) primarily highlighted genes involved in DNA damage repair mechanisms as modifiers of age at onset and disease severity, consistent with evidence that more DNA repair genes are being implicated in late age-onset neurodegenerative diseases. This provides an exciting opportunity to advance therapeutic development in HD, as these pathways have already been under intense investigation in cancer research. Also emerging are the roles of other polyglutamine disease proteins in DNA damage repair mechanisms. A potential universal trigger of oxidative DNA damage shared in these late age-onset diseases is the increase of reactive oxygen species (ROS) in human aging, defining an age-related mechanism that has defied other hypotheses of neurodegeneration. We discuss the potential commonality of DNA damage repair pathways in HD and other neurodegenerative diseases. Potential targets for therapy that may prove beneficial across many of these diseases are also identified, defining nodes in the ataxia telangiectasia-mutated (ATM) complex, mismatch repair, and poly ADP-ribose polymerases (PARPs).
Identifiants
pubmed: 31364066
doi: 10.1007/s13311-019-00768-7
pii: 10.1007/s13311-019-00768-7
pmc: PMC6985310
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
948-956Références
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