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Fig. 3 | Alzheimer's Research & Therapy

Fig. 3

From: Tau passive immunization blocks seeding and spread of Alzheimer hyperphosphorylated Tau-induced pathology in 3 × Tg-AD mice

Fig. 3

Alzheimer’s disease abnormally hyperphosphorylated Tau (AD p-Tau) seeds and templates the host Tau into neurofibrillary pathology at 7.5 weeks after AD p-Tau injection in triple-transgenic Alzheimer’s disease (3 × Tg-AD) mice. AD p-Tau (0.35 μg/2.5 μl saline), or saline (2.5 μl) as vehicle control, was unilaterally injected into the right hippocampus of 11- to 12-month-old female 3 × Tg-AD mice, and the mice were perfused at 7.5 weeks after injection. a AT8 and thioflavin-S staining in the 3 × Tg-AD mice injected with saline and treated with 43D. b AT8 and thioflavin-S staining in CA1 and subiculum in the 3 × Tg-AD mice injected with AD p-Tau and treated with mouse immunoglobulin G (IgG). c AT8 and thioflavin-S staining in naive 18-month-old female 3 × Tg-AD mice. d Double-immunofluorescence staining with AT8 and anti-amyloid-β (anti-Aβ) (D54D2) in brain sections of mice injected with AD p-Tau and treated with control mouse IgG. Tangle-bearing neurons (dashed circles) showed neither Aβ-positive filamentous inclusions nor increased Aβ somatodendritic immunoreactivity as compared with tangle-free neurons (dotted circles). Aβ staining was thresholded using Yen’s arithmetic and quantified using ImageJ software, and results were expressed as average percentage area occupied by Aβ staining in the somatodendritic compartment of tangle-bearing neurons compared with adjacent tangle-free neurons at × 60 magnification (n = 3 mice). High-magnification views of the boxed regions are shown as insets. Arrows = tangles; arrowheads = Aβ plaques. *P < 0.05, paired t test. Scale bars = 100 μm (ac) and 20 μm (d)

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