Fig. 8From: Myeloid deficiency of the intrinsic clock protein BMAL1 accelerates cognitive aging by disrupting microglial synaptic pruningSleep–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 timeBack to article page