Indeed, astrocytic UPR activation leads to a reactive state that contributes to neurodegeneration via reduced trophic support to neurons via an altered secretome resulting from reduced translation rates.24 Co-labelling with FUNCAT and the astrocytic marker, GFAP, in CA1 sections revealed marked repression of the nascent proteome in astrocytes in prion-disease, consistent with our previous findings,24 which was restored by treatment with trazodone [Fig. 1G(i–vi)]. The gene discussed is GFAP; the disease is prion disease.