Glial MARK2 Modulate Inflammatory Signaling and Protects Against Tau‐induced Neurodegeneration

This study identifies a previously unrecognized function of MARK2/Par-1 in inflammatory cytokine expression in glial cells. Reduced activity of MARK2 might cause excessive glial activation and exacerbate neurodegeneration. These findings provide insight into the molecular underpinnings of glial inflammation in AD and highlight MARK2 as a potential therapeutic target for modulating neuroinflammatory responses.