While existing mathematical models of AD predominantly address various known features of the disease, including (1) the development of potential AD treatments [16], [17]; (2) the dysrhythmic behavior of inhibitory neurons triggered by AD [18]; (3) the influence of the APOE4 gene on AD onset [19], [20]; (4) the temporal evolution of AD biomarkers [21], [22]; (5) interactions among brain cells and these plaques [23]–[26]; and (6) the formation of $\mathbb{ A_\beta }$ fibrils and plaques [27]. The gene discussed is APOE; the disease is Alzheimer disease.