Further novel contributions of interest include: demonstrating qualitative properties of disease propagation and damage, in primary and secondary tauopathy (Results, A simplified model of Alzheimer’s disease proteopathy), using globally constant, but non-physical, parameters; and demonstrating that the model can achieve tau distributions that reflect canonical patterns in Alzheimer’s patient data (Results, A mixed model comparison to Alzheimer’s diseased patient data). This evidence concerns the gene MAPT and proteostasis deficiencies.