Objective：To investigate the effects and molecular mechanisms of Nao Tan Qing（NTQ）on neural stem cell（NSC） proliferation in Alzheimer’s disease（AD）mice. Methods：Transgenic mice with five familial Alzheimer’s disease（5 × FAD）were randomly assigned to two groups，the AD group treated with ddH2O and AD + NTQ group administered with NTQ by gavage. Immunofluorescence staining，real -time quantitative PCR（RT -qPCR），and Western blot were used to evaluate NSC proliferation in hippocampus. In vitro，embryonic NSCs of C57/BL6J mice were isolated and cultured with PBS or NTQ. Cell proliferation was detected by CCK -8 method and cell apoptosis was analyzed by TUNEL. Immunofluorescence staining was used to detect the number of sex - determing region of Y chromosome（SOX2）- box transcription factor 2（SOX2）positive，5 - bromo - 2 - deoxy uridine（BrdU）positive， and doublecortin（DCX）positive cells. The mRNA and protein levels of SOX2 and DCX were measured by RT-qPCR and Western blot. The expressions of cyclin D1，p27/Kip1 and GATA2 were detected by RT-qPCR and Western blot. The expression level of SOX2 was detected by RT-qPCR and Western blot after the in vitro treatment of NSC using cyclin D1-cyclin-dependent kinase（CDK）inhibitor. Results：In the AD+NTQ group，the number of SOX2+ cells in hippocampus significantly increased，with a marked elevation in SOX2 mRNA and protein levels compared with the AD group. In vitro，the diameter of neurospheres treated with NTQ was significantly larger， along with the increased number of BrdU+ ，SOX2 + ，and DCX+ cells. Moreover，SOX2 and DCX mRNA levels，as well as SOX2 protein level，were notably elevated. Mechanistically，the expression of GATA2 and its downstream molecule p27/Kip1 were decreased in the hippocampus of AD+NTQ mice，and the inhibitory effect on cyclin D1 was weakened in NSC proliferation. Addition of cyclin D1-CDK inhibitor attenuated the increase in SOX2 and DCX expression triggered by NTQ. Conclusion：NTQ maintains NSC proliferation and alleviates cognitive deficits in AD mice by modulating the GATA2-p27/Kip1-cyclin D1 signaling pathway.