Abstract
Age-associated dysregulation of sleep can be worsened by Alzheimer's disease (AD). AD and sleep restriction both impair cognition, yet it is unknown if mild chronic sleep restriction modifies the proteopathic processes involved in AD. The goal of this work was to test the hypothesis that sleep restriction worsens memory impairments, and amyloid β-peptide (Aβ) and pTau accumulations in the brain in a mouse model of AD, with a focus on a role for circulating glucocorticoids (GC). Male 3xTgAD mice were subjected to sleep restriction (SR) for 6 h/day for 6 weeks using the modified multiple platform technique, and behavioral (Morris water maze, fear conditioning, open field) and biochemical (immunoblot) outcomes were compared to mice undergoing daily cage transfers (large cage control; LCC) as well as control mice that remained in their home cage (control; CTL). At one week, both LCC and SR mice displayed significant elevations in plasma corticosterone compared to CTL (p
Original language | English (US) |
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Pages (from-to) | 200-208 |
Number of pages | 9 |
Journal | Brain Research |
Volume | 1529 |
DOIs | |
State | Published - Sep 5 2013 |
Externally published | Yes |
Keywords
- Alzheimer's disease
- Amyloid
- Fear conditioning
- Glucocorticoids
- Morris water maze
- Sleep restriction
ASJC Scopus subject areas
- General Neuroscience
- Clinical Neurology
- Developmental Biology
- Molecular Biology
- General Medicine