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. 2015 Jul 3;78(3):426–438. doi: 10.1002/ana.24453

Figure 4.

Figure 4

Neural‐specific ablation of C9orf72 does not cause signs of neuroinflammation or other pathological hallmarks of amyotrophic lateral sclerosis in 18‐month‐old Nestin‐Cre+/−;C9orf72fl/fl mice. (A–D) Immunofluorescent staining of adult spinal cord using anti–glial fibrillary acidic protein (GFAP) or anti‐Iba1 antibodies. Graphs show quantification of GFAP‐ or Iba1‐positive areas. No signs of gliosis are observed in Nestin‐Cre+/−;C9orf72fl/fl mice. (E, F) Immunofluorescent staining of adult spinal cord using anti–TDP‐43 antibodies. Nuclear TDP‐43 staining is detected in Nestin‐Cre+/−;C9orf72fl/fl mice and control littermates. (G, H) Representative images showing immunostaining for ubiquitin in adult spinal cord. Ubiquitin expression is not affected by loss of C9orf72. Data in graphs represent mean ± standard deviation, n = 3 per genotype. Scale bars: A, C, G, 100μm; E, 30μm. DAPI = 4′,6‐diamidino‐2‐phenylindole; GM = gray matter; WM = white matter.