Accordingly, a large Aβ plaque burden with characteristic dense-core plaques was observed throughout the brain of AD mice, including the hippocampus, cortex, olfactory bulb and amygdala, with no deposits present in the cerebellum and the brainstem (Fig. 6A), thereby consistent with the previously reported forebrain parenchymal amyloidosis for this Tet-off APP mouse model [42]. The gene discussed is APP; the disease is amyloidosis.