Fig. 1.

Pathology of CTE, examples from the CTE cohort. 50 μm free-floating coronal sections were stained with mouse monoclonal antibody (AT8; Pierce Endogen) for phosphorylated tau (p-tau). For all microscopic images, 10 μm paraffin-embedded tissue sections were stained with AT8. Positive p-tau staining appears dark red, hematoxylin counterstain. Magnification is ×400. Stage I: Case 6. 23-Year-old NFL player with isolated CTE lesion in frontal cortex (red rectangle, top); corresponding perivascular CTE p-tau lesion at the depths of the superior frontal sulcus (red rectangle, bottom). Stage II: Case 13. 25-Year-old former college football player with 3 CTE lesions in frontal cortex (red rectangle, top); corresponding perivascular CTE p-tau lesion at depth of the sulcus in dorsolateral frontal cortex (red rectangle, bottom). Stage III: Case 19. 50-Year-old former NFL player with multiple, large confluent CTE lesions in the frontal, parietal and temporal cortices and diffuse neurofibrillary degeneration of entorhinal cortex and amygdala (red rectangle, top); corresponding perivascular CTE p-tau lesion at depths of the sulcus in dorsolateral frontal cortex (red rectangle, bottom). Stage IV: Case 31. 68-Year-old former NFL player with large confluent CTE lesions involving most of the frontal, insular and temporal cortex, there is severe diffuse p-tau deposition in the amygdala and entorhinal cortex (red rectangle, top); corresponding perivascular CTE p-tau lesion at depths of the sulcus in dorsolateral frontal cortex (red rectangle, bottom)