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Figure 2 | Acta Neuropathologica Communications

Figure 2

From: Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer’s disease

Figure 2

Aβ/C99 immunoreactivity in dorsal subiculum, CA1 and RSG of Tg APParc mice that have undergone partial destruction of the subiculum. A. Tg APParc mice aged 3 months comparing lesioned and intact hemispheres in the dorsal subiculum and CA1 of Tg mice injected with PBS (TG + PBS), Tg mice injected with ibotenic acid (TG + Ibo) and WT mice injected with ibotenic acid (WT + Ibo). We observed decreased Aβ pathology in both the dorsal subiculum and CA1 in Tg mice injected with ibotenic acid (Tg + Ibo). B. Aβ/C99 immunoreactivity in dorsal subiculum, CA1 and RSG of lesioned Tg APParc mice aged 6 months. Tg mice with ibotenic acid lesions have decreased Aβ/C99 immunoreactivity in the dorsal subiculum, CA1 and RSG. C. Quantification of the Aβ/C99 immunoreactivity comparing Aβ/C99 immunoreactivity (Aβ IR) in the lesioned hemisphere as a percentage of the contralateral side. Tg mice with ibotenic acid lesions have significantly decreased Aβ/C99 immunoreactivity in the damaged hemisphere in the dorsal subiculum and CA1 at ages 3 and 6 months. D. Plots representing cell count in the subiculum (percentage of contralateral side) vs. Aβ/C99 immunoreactivity in Tg + Ibo animals for the dorsal subiculum, CA1 and RSG of mice aged 3 and 6 months. Plots indicate a no correlation, rs = 0.2, p > 0.05 (3 and 6 months dorsal subiculum, CA1 and RSG). Data expressed as means ± SEM. Asterisk denotes statistical significance (*p < 0.05).

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