In vivo studies performed on trihexyphenidyl-treated rats and 3xTg-AD mice showed that AF710B can restore cognitive deficits and attenuate signs of AD phenotypes by the reduction of β-secretase 1 (BACE1) levels, GSK3β and CDK5/p25 activity (which contribute to the hyperphosphorylation of tau protein), neuroinflammation, soluble and insoluble Aβ40 and Aβ42 plaques, and tau pathology [82]. Here, BACE1 is linked to Alzheimer disease.