Although it is not the only additional aspect that could be implemented in the model due to its impact on AD progression (e.g., vascular damage leading to reduced protein clearance, infections such as herpes virus, genetic factors, etc.), we expect that by including these glial effects, we could reproduce the slight decay in hp-tau concentration that is found in the literature, but not reproduced in our results. The gene discussed is MAPT; the disease is Alzheimer disease.