Previously, we created an HFSTZ APP/PS1 animal model, which displayed diabesity and hepatic steatosis; elevated peripheral Aβ level; enhanced Aβ level, plaque burden, astrocyte activation, vascular inflammation, glucose hypometabolism in the cerebrum, and caused cognitive impairment in APP/PS1 mice [3,4]. The gene discussed is APP; the disease is Cognitive impairment.