Figure 2. Pathological features in the brain of Coq9 ^R239X mice after β‐RA treatment.

• A–U
  (A₁–F₁) H&E stain in the diencephalon of Coq9 ^+/+ mice (A₁ and D₁), Coq9 ^R239X mice (B₁ and E₁), and Coq9 ^R239X mice after β‐RA treatment (C₁ and F₁). (G₁–L₁) Anti‐GFAP stain in the diencephalon of Coq9 ^+/+ mice (G₁ and J₁), Coq9 ^R239X mice (H₁ and K₁), and Coq9 ^R239X mice after β‐RA treatment (I₁ and L₁). (M₁–R₁) Anti‐Iba1 stain in the diencephalon of Coq9 ^+/+ mice (M₁ and P₁), Coq9 ^R239X mice (N₁ and Q₁), and Coq9 ^R239X mice after β‐RA treatment (O₁ and R₁). (S₁–U₁) Protein oxidation in the diencephalon of Coq9 ^+/+ mice (S₁), Coq9 ^R239X mice (T₁), and Coq9 ^R239X mice after β‐RA treatment (U₁). (A₂–C₂) Magnetic Resonance Images of the diencephalon of Coq9 ^+/+ mice (A₂), Coq9 ^R239X mice (B₂), and Coq9 ^R239X mice after β‐RA treatment (C₂). (D₂–F₂) Magnetic Resonance Images of the pons of Coq9 ^+/+ mice (D₂), Coq9 ^R239X mice (E₂), and Coq9 ^R239X mice after β‐RA treatment (F₂). (G₂–I₂) Lactate peak in the brain of Coq9 ^+/+ mice (G₂), Coq9 ^R239X mice (H₂), and Coq9 ^R239X mice after β‐RA treatment (I₂). Scale bars: 1 mm (A₁–C₁); 100 μm (D₁–F₁); 200 μm (G₁–I₁); 100 μm (J₁–L₁); 200 μm (M₁–O₁); 100 μm (P₁–R₁); 100 μm (S₁–U₁). The yellow arrows indicated the areas of increased T2 signal, which is characteristic of lesions in specific brain areas.