Dose-dependent phosphorylation of endogenous Tau by intermittent hypoxia in rat brain.
Alzheimer’s disease
Tau phosphorylation
intermittent hypoxia
sleep apnea
Journal
Journal of applied physiology (Bethesda, Md. : 1985)
ISSN: 1522-1601
Titre abrégé: J Appl Physiol (1985)
Pays: United States
ID NLM: 8502536
Informations de publication
Date de publication:
01 09 2022
01 09 2022
Historique:
pubmed:
22
7
2022
medline:
1
9
2022
entrez:
21
7
2022
Statut:
ppublish
Résumé
Intermittent hypoxia, or intermittent low oxygen interspersed with normal oxygen levels, has differential effects that depend on the "dose" of hypoxic episodes (duration, severity, number per day, and number of days). Whereas "low dose" daily acute intermittent hypoxia (dAIH) elicits neuroprotection and neuroplasticity, "high dose" chronic intermittent hypoxia (CIH) similar to that experienced during sleep apnea elicits neuropathology. Sleep apnea is comorbid in >50% of patients with Alzheimer's disease-a progressive, neurodegenerative disease associated with brain amyloid and chronic Tau dysregulation (pathology). Although patients with sleep apnea present with higher Tau levels, it is unknown if sleep apnea through attendant CIH contributes to onset of Tau pathology. We hypothesized CIH characteristic of moderate sleep apnea would increase dysregulation of phosphorylated Tau (phospho-Tau) species in Sprague-Dawley rat hippocampus and prefrontal cortex. Conversely, we hypothesized that dAIH, a promising neurotherapeutic, has minimal impact on Tau phosphorylation. We report a dose-dependent intermittent hypoxia effect, with region-specific increases in
Identifiants
pubmed: 35861520
doi: 10.1152/japplphysiol.00332.2022
pmc: PMC9448341
doi:
Substances chimiques
Oxygen
S88TT14065
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
561-571Subventions
Organisme : NHLBI NIH HHS
ID : T32 HL134621
Pays : United States
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