APP/PS1 mice are a well-established animal model for studying Alzheimer’s disease; by introducing human APP and PS1 mutant genes, these mice produce excessive amyloid-β (Aβ), particularly the highly toxic Aβ42, which accumulates in brain tissue to form amyloid plaques and faithfully reproduces the early pathological features of AD. The gene discussed is PSEN1; the disease is Alzheimer disease.