Fig. 4
From: Common mouse models of tauopathy reflect early but not late human disease
Tau modification extent correlates with Tau pathology kinetics in both models and human AD. A-B Specific Tau regions and modification sites with high stoichiometry of modification are identified by unbiased data analyses. Euclidean hierarchical clustering of relative amounts of unmodified FLEX-peptide of insoluble Tau derived from the cortex of the P301S (A) and P301L model (B) shows regions with high modification extent. C Average extent of modification of FLEX-peptides per condition from insoluble Tau derived from the cortex of the P301S and P301L model ordered from N- to C-terminus. Arrows indicate regions that become highly modified when aggregates form. D-G Pearson correlation analyses are performed to study the extent of modification of specific peptides and the amount of insoluble Tau. 195–209 (D), 212–221 (E), 386–395 (F), 396–406 (G). This correlation analyses are performed for the cortex of the P301S and P301L model and the BA39 of human AD (human AD data is adapted from [20]). H-J Pearson correlation of singly phosphorylated peptides with insoluble Tau in the cortex of the P301S and P301L models. Phosphorylated peptides 195–209 (H), 212–221 (I), 396–406 (J) also show a strong association with disease