Figure 4.
Propagation of tau pathology after inoculation of a lower dose of AD-tau into young and aged non-Tg mice. (A) AT8 immunostaining for various brain regions after a lower dose of AD-tau inoculation (2 µg/mouse) into the dorsal hippocampus (HP) and overlying cortex of 2–3-mo-old non-Tg mice (C57BL6). Only weak AT8 immunoreactivities were detected in the ipsilateral (Ipsi) ventral hippocampus at 1 mo p.i. (three mice). More prominent AT8-positive tau inclusions appeared in both the ipsilateral and contralateral (Contra) ventral hippocampus at 3 mo p.i. (three mice), which showed a trend of decline between 6 and 9 mo p.i. (four and three mice, respectively). Bar, 100 µm. (B) Quantification of percent area occupied by AT8-positive tau pathology developed in the ventral hippocampal hilus with 2-µg AD-tau injection (three to four mice per time point; each dot represents one mouse). (C) Quantification of NeuN+ cells in the ventral hippocampal hilus region with 2-µg AD-tau injection. Data are shown as mean + SEM. (B and C) One-way ANOVA showed no significant differences among groups. (D) Comparisons of AT8-positive tau pathology developed in the ipsilateral entorhinal cortex, ipsilateral fimbria, and corpus callosum at 6 mo p.i. of AD-tau into young (2–3 mo) versus aged (15–19 mo) non-Tg mice (2 µg/mouse; four young and three aged mice at 6 mo p.i. with each dot representing one mouse; all C57BL6). Bar, 100 µm. (E–G) Quantification of percent area occupied by AT8 immunoreactivities in regions shown in D followed by Student’s t tests indicated that aged mice developed significantly more pathology in the ipsilateral entorhinal cortex (*, P < 0.05) and a trend of more abundant pathology in the ipsilateral fimbria and corpus callosum. Data represent three to four mice per time point; each dot represents one mouse.