A role for gliosis and neuroinflammation in Tauopathy is evidenced by greater microglial activity and altered inflammatory pathway markers (e.g., interleukin-6, tumor necrosis factor-α) correlating with Tau burden [56–59] as well as inflammation-related AD risk factors that contribute to Tauopathy such the genetic factors of TREM2 [60] and APOE4 [61] and the environmental factors of traumatic brain injury [62, 63] and viral infection [64, 65]. This evidence concerns the gene APOE and viral infectious disease.