Breast cancer type 1 and neurodegeneration: consequences of deficient DNA repair.
BRCA1
DNA damage
DNA repair
neurodegeneration
senescence
Journal
Brain communications
ISSN: 2632-1297
Titre abrégé: Brain Commun
Pays: England
ID NLM: 101755125
Informations de publication
Date de publication:
2021
2021
Historique:
received:
15
03
2021
revised:
09
04
2021
accepted:
13
04
2021
entrez:
5
7
2021
pubmed:
6
7
2021
medline:
6
7
2021
Statut:
epublish
Résumé
Numerous cellular processes, including toxic protein aggregation and oxidative stress, have been studied extensively as potential mechanisms underlying neurodegeneration. However, limited therapeutic efficacy targeting these processes has prompted other mechanisms to be explored. Previous research has emphasized a link between cellular senescence and neurodegeneration, where senescence induced by excess DNA damage and deficient DNA repair results in structural and functional changes that ultimately contribute to brain dysfunction and increased vulnerability for neurodegeneration. Specific DNA repair proteins, such as breast cancer type 1, have been associated with both stress-induced senescence and neurodegenerative diseases, however, specific mechanisms remain unclear. Therefore, this review explores DNA damage-induced senescence in the brain as a driver of neurodegeneration, with particular focus on breast cancer type 1, and its potential contribution to sex-specific differences associated with neurodegenerative disease.
Identifiants
pubmed: 34222870
doi: 10.1093/braincomms/fcab117
pii: fcab117
pmc: PMC8242133
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
fcab117Informations de copyright
© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.
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