We present a multiscale model for the onset and evolution of AD which accounts for the diffusion and agglomeration of amyloid-β (Aβ) peptide (amyloid cascade hypothesis [15, 21]), and the spreading of the disease through neuron-to-neuron transmission (prionoid hypothesis [7]). The model is a conceptual interdisciplinary construction based on clinical and experi- mental evidence, yielding in particular numerical simulations and related graphs, that can be compared with time-dependent trajectories of AD biomarkers [19, 20].