Senescence-related impairment of autophagy induces toxic intraneuronal amyloid-β accumulation in a mouse model of amyloid pathology.
Alzheimer’s disease
Autophagy
Cellular senescence
Intraneuronal Aβ
Telomere shortening
Journal
Acta neuropathologica communications
ISSN: 2051-5960
Titre abrégé: Acta Neuropathol Commun
Pays: England
ID NLM: 101610673
Informations de publication
Date de publication:
17 05 2023
17 05 2023
Historique:
received:
05
05
2023
accepted:
07
05
2023
medline:
19
5
2023
pubmed:
18
5
2023
entrez:
17
5
2023
Statut:
epublish
Résumé
Aging is the main risk factor for Alzheimer's disease (AD) and other neurodegenerative pathologies, but the molecular and cellular changes underlying pathological aging of the nervous system are poorly understood. AD pathology seems to correlate with the appearance of cells that become senescent due to the progressive accumulation of cellular insults causing DNA damage. Senescence has also been shown to reduce the autophagic flux, a mechanism involved in clearing damaged proteins from the cell, and such impairment has been linked to AD pathogenesis. In this study, we investigated the role of cellular senescence on AD pathology by crossing a mouse model of AD-like amyloid-β (Aβ) pathology (5xFAD) with a mouse model of senescence that is genetically deficient for the RNA component of the telomerase (Terc
Identifiants
pubmed: 37198698
doi: 10.1186/s40478-023-01578-x
pii: 10.1186/s40478-023-01578-x
pmc: PMC10189946
doi:
Substances chimiques
Amyloid beta-Peptides
0
Amyloid beta-Protein Precursor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
82Informations de copyright
© 2023. The Author(s).
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