In line with this hypothesis, IL-1β can also cause an imbalance between the GABAergic and glutamatergic synaptic transmission at Purkinje cell synapses in experimental autoimmune encephalomyelitis (EAE) cerebellum, which are early events triggering secondary excitotoxicity and inflammatory neurodegeneration in EAE disease [48, 49]. Here, IL1B is linked to experimental autoimmune encephalomyelitis.