Fig 5

Alzheimer’s disease abnormally hyperphosphorylated Tau (AD p-Tau) injection accelerates the development of amyloid-β (Aβ) plaques in triple-transgenic Alzheimer’s disease (3 × Tg-AD) mice. AD p-Tau (0.35 μg in 2 μl of saline) isolated from autopsied AD cerebral cortex was unilaterally injected into the right hippocampus of 11- to 12-month-old female 3 × Tg-AD mice or saline as a vehicle control. The mice were perfused at 7.5 weeks after AD p-Tau injection, and the coronal sections were stained with thioflavin-S. a Representative images of thioflavin-S staining of plaques in the contralateral and ipsilateral subiculum of mice in the AD p-Tau/immunoglobulin G (IgG) group. b Plaque areas in the contralateral and ipsilateral sides of the brain were calculated at × 10 magnification from 22 to 25 serial coronal sections per mouse in AD p-Tau/43D (n = 6) and AD p-Tau/IgG (n =7) groups. **P < 0.01, paired t test. c Representative images of thioflavin-S staining of plaques in the ipsilateral subiculum of the mice in saline/43D, AD p-Tau/IgG, and AD p-Tau/IgG groups. d Plaque areas were calculated at × 10 magnification from 22 to 25 serial coronal sections per mouse (every fourth section of the brain) in mice treated with saline/43D (n = 6), AD p-Tau/IgG (n = 7), and AD p-Tau/43D (n = 6). e Plaque areas in the contralateral and ipsilateral hippocampus in saline/43D mice (n = 6) and in the ipsilateral hippocampus in AD p-Tau/43D or IgG (n = 13) were measured at × 10 magnification from 22 to 25 serial coronal sections per mouse (every fourth section of the brain). A two-tailed t test was used for ipsilateral side between saline/43D and AD p-Tau/43D and AD p-Tau/IgG mice. A paired t test was used between contralateral and ipsilateral hippocampus of saline/43D mice. *P < 0.05