Fig. 5.
PrP-induced tau phosphorylation in cortex of inherited prion diseases: upper row deposition of abnormal PrP in the frontal cortex; there is considerable variability of the intensity of PrPSc burden and some forms are characterised by distinct patterns of plaque formation, as described before. The lower row shows tau deposits corresponding to the area depicted above. A, 96 bp OPRI mutation with almost undetectable PrPSc load, resulting in tau phosphorylation similar to the 144 bp OPRI (f, g), despite its significantly higher PrPSc load (b). c This case with a P102L mutation shows predominantly diffuse deposits and only very few plaques, as compared to the very heavily plaque-forming A117V case (d), both showing similar tau hyperphosphorylation (h, i). Another case with no plaque formation, E200K (e), shows a tau load similar to all other cases (j). Scale bar a–e 240 μm, f–j 60 μm