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. Author manuscript; available in PMC: 2016 Jan 15.
Published in final edited form as: Cell. 2015 Jan 15;160(0):177–190. doi: 10.1016/j.cell.2014.12.019

Figure 7. LD accumulation is present in the astrocytes and microglia of Ndufs4−/− mice prior to neurodegeneration.

Figure 7

A) a–d 20µm coronal cryosections reveal LD accumulation in the VN and OB of Ndufs4−/− mice compared to control (C57Bl/6). e–h LD accumulates in the astrocytes and microglia of the VN and OB shown by colocalization with the astrocyte marker, GFAP and the microglia marker, Iba1. (B) LD accumulation in the VN is high in the P23 mutants but decreases in number in the P34 and >P50 mutants. (C) In the OB, LD accumulation occurs in the P23 mutants and increases in number in the P34 and >P50 animals. (D) Ndufs4−/− exhibit elevated triglyceride (TAG) levels in the OB in an age-dependent manner. E) pJNK is increased in the mutants. Right panels show the quantification of the immunoblots. F) Neuronal knockdown of dNdufs4 (CG12203) leads to LD accumulation in the glia, while glial knockdown results in no LD accumulation. (*P<0.05, **P<0.005, ***P<0.0005). G) Quantification of F. H) 7-day administration of AD4 in P21 animals via IP injection at 150mg/kg shows treated mutant animals with improved clinical signs (body weight loss, hypotonia, ataxia, piloerection, clasping, gasping, paralysis, tremor) upon aging and I) performing at a comparable level as control while mutants treated with saline show progressive decline in motor performance. (*p<0.05 KO SAL vs KO AD4, two-way ANOVA). See also Figure S7.