Studies from other neuroinflammatory models, such as experimental autoimmune encephalomyelitis (EAE), have indicated that reactive, GFAP-positive astrocytes can have impaired glutamate metabolism, with decreased action of glutamate dehydrogenase and glutamine synthetase, which results in higher glutamate concentration and potential excitotoxicity [27]. The gene discussed is GFAP; the disease is experimental autoimmune encephalomyelitis.