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Fig. 1 | Journal of Neuroinflammation

Fig. 1

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

Fig. 1

Microglia BMAL1 deficiency disrupts hippocampal-dependent behavior and increases anxiety in aged, but not young mice. A Preference in the novel object recognition task in young (3–6 months, CD11bcre, n = 15; CD11bcre;Bmal1lox/lox, n = 12) and aged (18–20 months, CD11bcre, n = 10; CD11bcre;Bmal1lox/lox, n = 16) mice. B Primary escape latency during the 5-day trial period for young and aged mice. C Escape latency in the testing phase of the Barnes maze task in young (3–6 months, CD11bcre, n = 6; CD11bcre;Bmal1lox/lox, n = 6) and aged (18–20 months, CD11bcre, n = 9; CD11bcre;Bmal1lox/lox, n = 10) mice. D Distance travelled in whole arena in the open field task in young (3–6 months, CD11bcre, n = 21; CD11bcre;Bmal1lox/lox, n = 17) and aged (18–20 months, CD11bcre, n = 12; CD11bcre;Bmal1lox/lox, n = 19) mice. E Time spent in the center area in the open field task in young (3–6 months, CD11bcre, n = 21; CD11bcre;Bmal1lox/lox, n = 17) and aged (18–20 months, CD11bcre, n = 12; CD11bcre;Bmal1lox/lox, n = 19) mice. Data are represented as the mean ± SEM. P-values were calculated using paired t-test, or two-tailed Student’s t-test.

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