Activation of the hypoxia response protects mice from amyloid-β accumulation.
Alzheimer’s disease
HIF
Hypoxia
Inflammation
Metabolism
Vascularity
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
19 Jul 2022
19 Jul 2022
Historique:
received:
05
01
2022
accepted:
29
06
2022
revised:
27
06
2022
entrez:
19
7
2022
pubmed:
20
7
2022
medline:
22
7
2022
Statut:
epublish
Résumé
Alzheimer's disease (AD) is the most common cause of dementia with limited treatment options affecting millions of people and the prevalence increasing with the aging population. The current knowledge on the role of the hypoxia/hypoxia-inducible factor (HIF) in the AD pathology is restricted and controversial. We hypothesized based on benefits of the genetic long-term inactivation of HIF prolyl 4-hydroxylase-2 (HIF-P4H-2) on metabolism, vasculature and inflammatory response that prolonged moderate activation of the hypoxia response could hinder AD pathology. We used an aging model to study potential spontaneous accumulation of amyloid-β (Aβ) in HIF-P4H-2-deficient mice and a transgenic APP/PSEN1 mouse model subjected to prolonged sustained environmental hypoxia (15% O
Identifiants
pubmed: 35852609
doi: 10.1007/s00018-022-04460-6
pii: 10.1007/s00018-022-04460-6
pmc: PMC9296391
doi:
Substances chimiques
Amyloid beta-Peptides
0
Amyloid beta-Protein Precursor
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
432Subventions
Organisme : Terveyden Tutkimuksen Toimikunta
ID : 266719
Organisme : Terveyden Tutkimuksen Toimikunta
ID : 308009
Organisme : Terveyden Tutkimuksen Toimikunta
ID : 296498
Organisme : Terveyden Tutkimuksen Toimikunta
ID : 251314
Organisme : Academy of Finland
ID : 284605
Informations de copyright
© 2022. The Author(s).
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