They found that Aβ pathology could promote tau propagation over the neocortex by enhancing the microglial activation, suggesting microglial activation as a key factor to link Aβ pathology and tau spread, proposing that the simultaneous appearance of Aβ protein, tau tangles, and abnormal microglial activation may synergize to drive the occurrence and progression of AD [34]. The gene discussed is MAPT; the disease is Alzheimer disease.