GFAP and Alzheimer disease: Likely due to TA-3-mediated downregulation of Tau or Aβ that can induce inflammasome activation 57, neuroinflammation evidenced by increased numbers of GFAP+ astrocytes and Iba1+ microglial cells, key players in neuroinflammation of AD 58, 59 was significantly diminished by TA-3 treatment (Figure 6F-G).