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. 2008 Mar;172(3):786–798. doi: 10.2353/ajpath.2008.070904

Figure 4.

Figure 4

Comparison of tauopathy in biAT and biGT mice relative to parental Tau-P301L mice. Each horizontal panel (A–D) compares by representative pictures, different aspects of the tauopathy in different brain regions of APP-V717I × Tau-P301L mice (middle) and GSK-3β × Tau-P301L mice (right) relative to the parental Tau-P301L mice (left). IHC with mAb AT100 shown for hippocampus CA1 (A), cortex (B), and brainstem (C) and with pAb PY18 in cortex (D). Note: mAb AT100 always yields some nuclear staining because of weak cross-reaction with a nuclear phospho-protein present in all brain cells, not related to protein tau. Insets in B show higher magnifications of single neurons to illustrate the highly neurofibrillary aspect of tangles in both bigenic mouse strains at old age (14 to 18 months) as opposed to the more diffuse aspect in the parental Tau-P301L mice, which are evidently younger (and see text).29 The fibrillar morphology of the tangles is demonstrated by ultrastructural analysis of tau filaments in GSK-3β × Tau-P301L bigenic mice (E) and after immunogold labeling with mAb AT8 (F). Scale bars: 100 μm (A–D); 5 nm (E); 200 nm (F).