While TXL intervention could obviously restore AQP-4 polarization and abate Aβ accumulation and the formation of Aβ1–42 oligomers, indicating the blocking effects of TXL on the potential vicious circle between the astrocytic pyroptosis and Aβ accumulation after reperfusion, which provides not only detailed action principle for protective effects of TXL against cerebral I/R induced BBB damage but biological evidence for the potential efficacy of preventing and treating poststroke dementia by TXL in clinical practice. This evidence concerns the gene AQP4 and dementia.