Figure 4.
Plaque distribution in telencephalic areas of APdE9 mice. Anti-human Aβ staining (W0-2) in APdE9 mice at the end of the study (age, 5 months) revealed a substantial number of amyloid plaques in the cortex, hippocampus, and amygdala, but hardly any plaques in the thalamus. A–D, The coronal sections of an APdE9 mouse are at the levels of motor cortex (A), amygdala and perirhinal cortex (B), septal hippocampus (C), and dorsal thalamus just below the septal hippocampus (D). E, A corresponding hippocampal section of a wild-type mouse showing even no intracellular staining for human Aβ. Scale bars, 500 μm. F, Amyloid burden expressed as immunoreactive surface area in the percentage of the total area of analyzed sections. Student's t test did not reveal significant differences in plaque load between APdE9 mice with or without seizures for motor, perirhinal, and entorhinal cortices (p = 0.34), hippocampus (p = 0.34), and amygdala (p = 0.08). *In the thalamus, more APdE9 mice without seizures had plaques than mice with seizures (p = 0.01, Mann–Whitney U test). Cx, Perirhinal and entorhinal cortices; Hc, hippocampus; Am, amygdale; Th, thalamus.