To determine the vulnerability of two distinct cholinergic subpopulations in the disease progression of AD, we generated AD/TERM mice by crossing TERM mice with AD mice (APP/PS1 mice in a C57BL/6 genetic background), which displayed amyloid-β peptide (Aβ) plaques and neurofibrillary tangles similar with that seen in human patients (Duyckaerts et al., 2008; Bilkei-Gorzo, 2014; Kosel et al., 2020). The gene discussed is APP; the disease is Alzheimer disease.