Lack of the immune adaptor molecule SARM1 accelerates disease in prion infected mice and is associated with increased mitochondrial respiration and decreased expression of NRF2
Fig 4
The pattern of PrPSc deposition and spongiform change in the brain are similar at the clinical stage of disease in SARM1KO and C57Bl/6 mice inoculated IC with RML prions.
(A) PrPSc staining in the thalamus, cortex, and cerebellum (Cb) of clinically positive C57Bl/6 (155 DPI, left panels) and SARM1KO (148 DPI, right panels) mice inoculated IC with RML prions. PrPSc was detected using the anti-PrP rabbit monoclonal antibody EP1802Y as described in the materials and methods. (B) H&E staining of the thalamus, cortex, and cerebellum from clinically positive C57Bl/6 (155 DPI, left panels) and SARM1KO (148 DPI, right panels) mice inoculated intracranially with RML prions. For all panels, scale bar = 50μm.