To explore the role of FoxG1 in activating autophagy of AD model mice, we extended the in vivo studies by administering i.p. with TM to induce FoxG1 overexpression and simultaneously administering intracerebroventricularly (i.c.v.)with Aβ25–35 peptides in Cre/FoxG1fl/fl mice to induce AD vivo model. This evidence concerns the gene FOXG1 and Alzheimer disease.