A new preclinical study from Complutense University has found that CB1 receptor myelin repair mechanisms depend on intact endocannabinoid signaling at a critical cellular window. Researchers removed CB1 receptors specifically from newly formed oligodendrocytes in mice and observed that remyelination failed, neuroinflammation worsened, and motor recovery did not occur. While the findings are in animals and no cannabinoid was tested, they establish a specific mechanistic role for the endocannabinoid system in the brain’s ability to repair itself after injury.