We focused on the following mechanisms: (i) nodal stress, where highly connected nodes—the network hubs—experience more damage10-13; (ii) diffusion of disease effects proportionally to the weight of the outgoing connections7,14,15 and (iii) propagation of pathology throughout the brain.6,13,16-18 We also investigated the influence of apolipoprotein E (APOE)-ɛ4 carriage, the main genetic factor for Alzheimer’s disease, on these contributions. The gene discussed is APOE; the disease is Alzheimer disease.