ReviewFrontiers in neuroscience2026
Targeting microglia microtubules: cytoskeletal remodeling as a druggable hub in neuroinflammation and neurodegeneration.
Review in Frontiers in neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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4 authors.
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Abstract
Microglia dynamically remodel their cytoskeleton to surveil the brain, respond to injury, and shape synaptic connectivity. While actin drives rapid process motility and phagocytic cup formation, emerging evidence indicates that microtubules are critical regulators of microglial morphology, trafficking, and inflammatory signaling. In homeostatic microglia, microtubules are nucleated at Golgi outposts, supporting ramified architectures and low inflammatory tone. Upon activation, microglia undergo a switch to a centrosome-nucleated, radial microtubule array, driven in part by cyclin-dependent kinase 1 (Cdk1) and associated with polarized cytokine release, NLRP3 inflammasome engagement, and altered phagocytic behavior. We discuss how key regulators of this transition-including Cdk1, centrosomal γ-tubulin recruitment, Golgi-derived microtubule nucleation, and the kinase MARK4 may constitute druggable nodes to tune microglial reactivity in neuro-degenerative diseases. Finally, we outline experimental priorities for translating microglial microtubules into therapeutic targets.
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