ArticleBrain, behavior, & immunity - health2026
Microglia depletion alleviates the disruptions in circadian rhythms and anxiety caused by bmal1 deficiency.
Article in Brain, behavior, & immunity - health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Circadian control of immune homeostasis in cardiovascular health and disease.Frontiers in immunology · 2026Review
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7 authors.
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Abstract
Microglia, the intrinsic immune cells of the brain, play a crucial role in maintaining neuronal health and circadian rhythms. BMAL1 is a core transcriptional regulator of the molecular circadian clock that coordinates daily rhythms in physiology and behavior. In this study, we investigated the impact of microglial modulation on circadian disruptions and behavioral abnormalities observed in bmal-/- mice. Our results revealed disruptions in circadian rhythms and microglial activation in bmal-/- mice, characterized by altered activity patterns and increased microglia numbers. Inhibiting microglia with PLX5622 effectively ameliorated circadian disruptions and improved behavioral performance in bmal-/- mice, as observed in open field and elevated plus-maze tests. Additionally, microglia inhibition restored structural and functional abnormalities in neurons of bmal-/- mice, including dendritic spine reduction and impaired long-term potentiation (LTP). Furthermore, we observed a normalization of proinflammatory cytokine levels (IL-1β and TNF-α) upon PLX5622 treatment, indicating a potential link between microglial modulation and neuroinflammation. Our findings highlight the intricate interplay between circadian rhythms, microglia, and neuronal health, offering insights into potential therapeutic interventions for circadian-related and neuroinflammatory disorders.
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