Skip to main content
Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruning

Fig. 8

Sleep–wake behavior is disrupted in aged Bmal1 cKO mice. Baseline sleep–wake behavior was assessed over continuous 24-h recordings of aged CD11bcre (18–20 months; n = 6) and CD11bcre;Bmal1lox/lox (n = 7) mice under normal light–dark (12-h light:12-h dark) conditions. A–C Percentage of time spent in wake (A), NREM sleep (B), and REM sleep (C) across the entire 12-h light/dark period. D–F The average duration of individual wake (D), NREM (E), and REM (F) bouts across the entire 12-h light/dark phase. G–J The total number of wake (G), NREM (H), and REM (I) bouts across the 12-h light/dark phases. J Transitions between sleep–wake states across the 12-h light/dark phases. K The average REM bout latency during the 12-h light/dark periods. Data are represented as the mean ± SEM. P-values were calculated using two-tailed Student’s t-test or two-way ANOVA. ZT zeitgeber time

Back to article page