Amelioration of inflammatory response, down-regulation of the UPR effectors, and improvement of neuromotor abilities of Glb1^-/- mice after BMT. (A) Immunolabeling using an anti-SDF-1β antibody demonstrated that the level of this chemokine was lower in the thalamus of 6-month-old treated Glb1^-/- mice (Glb1^-/- BMT^β-gal) than in Glb1^-/- mice that underwent mock transplantation (Glb1^-/- BMT^GFP). Anti-GFAP staining demonstrated attenuation of reactive gliosis in the thalamus of 4-month-old treated Glb1^-/- mice. Immunolabeling with anti-F4/80 antibody showed that the proliferation and activation of microglia in the thalamus of 3-month-old treated Glb1^-/- mice were reverted to a resting state. Size bar corresponds to 50 μm. (B-C) CHOP and caspase-12 mRNA levels in the hindbrain, midbrain, and forebrain (HMF), brain stem (BS), cerebellum (CB), and spinal cord of treated Glb1^-/- mice (▪) were restored to levels that were comparable with those seen in wild-type tissues (▦). (D) Glb1^-/- mice that underwent transplantation (▪) performed better than untreated Glb1^-/- mice (▦) but not as well as wild-type mice (□) on the rotating rod test of motor coordination and balance (n = 15). (E) Similar results were seen on the open-field exploratory activity test (n = 17). Data are expressed as mean ± SD; groups were compared by one-way repeated measures ANOVA. ^#P < .05 relative to untreated Glb1^-/- littermates at the same age; post hoc Tukey test.