To evaluate this hypothesis, we orally administered the compound to an accelerated mouse model of cerebral amyloidosis [bearing amyloid precursor protein (APP) “Swedish” APPK595N/M596L (APPswe) and Presenilin 1 (PS1) exon 9 deleted (PS1ΔE9) mutant human transgenes; designated PSAPP mice] for 6 months, commencing at 6 months of age, and evaluated behavioral impairment, AD-like pathology, APP processing, neuroinflammation, and oxidative stress responses at 12 months of age. The gene discussed is PSEN1; the disease is Alzheimer disease.