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. 2013 Jan 28;136(1):28–42. doi: 10.1093/brain/aws322

Figure 6.

Figure 6

CR3/43, amyloid precursor protein and Luxol fast blue staining in the corpus callosum of representative cases with TBI versus control subjects. (A) CR3/43 (B) amyloid precursor protein and (C) Luxol fast blue staining in a 24-year-old male control subject who died following cardiomyopathy. Minimal CR3/43 immunoreactivity is accompanied by an absence of axonal pathology and white matter of a normal density and uniform distribution. Scale bars = 200 µm. (D) CR3/43 (E) amyloid precursor protein and (F) Luxol fast blue staining in a 37-year-old male who died 4 years post-TBI. Extensive amoeboid CR3/43 immunoreactivity is accompanied by multiple axonal bulbs and Luxol fast blue staining showing a decreased density of fibres and a non-uniform distribution of fibres within inflamed regions. Scale bars = 200 µm. (G) CR3/43 (H) amyloid precursor protein and (I) Luxol fast blue staining in a 43-year-old male who died 4 years post-TBI. Again, extensive amoeboid CR3/43 immunoreactivity is accompanied by minimal axonal pathology and a patchy loss of integrity of the white matter in association with regions of amoeboid microglia. Scale bars = 1 mm. (J) High magnification Luxol fast blue staining in the corpus callosum in the same case as A–C. (K) High magnification Luxol fast blue staining in the corpus callosum in the same case as D–F. (L) High magnification Luxol fast blue staining in the corpus callosum in the same case as G–I. Scale bars = 100 µm.