Sult and/or underlying pathology (Zamanian et al., 2012; Sirko et al., 2013). It is also possible that the relative contribution of astrocytes and CN/NFAT signaling to glial activation, and neuroinflammation in general, is greater in chronic disease conditions relative to acute injury. Regardless, the synaptoprotective effects of AAV-Gfa2-VIVIT, in the face of robust glial activation, suggests tha