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58 reviewsMeningeal lymphatics serve as an outlet for cerebrospinal fluid, and their dysfunction is associated withvarious neurodegenerative conditions. Previous studies have demonstrated that dysfunctional meningeallymphatics evoke behavioral changes, but the neural mechanisms underlying these changes have remainedelusive. Here, we show that prolonged impairment of meningeal lymphatics alters the balance of corticalexcitatory and inhibitory synaptic inputs, accompanied by deficits in memory tasks. These synaptic andbehavioral alterations induced by lymphatic dysfunction are mediated by microglia, leading to increasedexpression of the interleukin 6 gene (Il6). IL-6 drives inhibitory synapse phenotypes via a combination oftrans- and classical IL-6 signaling. Restoring meningeal lymphatic function in aged mice reverses age-associated synaptic and behavioral alterations. Our findings suggest that dysfunctional meningeal lymphaticsadversely impact cortical circuitry through an IL-6-dependent mechanism and identify a potential targetfor treating aging-associated cognitive decline.
