Abstract Background Bone morphogenetic proteins (BMPs) have been reported in many studies to be related to adult neurogenesis. Neurogenic impairment is a hallmark of Alzheimer’s disease (AD), while the involvement of BMPs remains unclear. Methods AD models were established using APP NL−G−F transgenic mice and C57BL/6 mice subjected to intracerebral injection of Aβ (25–35) peptide. Female APP NL−G−F mice received pharmacological inhibitor treatment, whereas Neuro2a cells were exposed to estrogen stimulation in vitro. Immunofluorescence staining was conducted to evaluate hippocampal neural stem cell proliferation. The hippocampus and cellular pellets were isolated, and quantitative PCR (qPCR) was employed to determine mRNA expression levels. Results Our study revealed that APP NL−G−F mice and Aβ-injected mice exhibited impaired neurogenesis in the brain, with a clear sex-dependent difference only in APP mice. Several BMPs were markedly upregulated in the hippocampus of AD model mice, with significantly higher expression in females than in males. BMP inhibitor attenuated neural stem cell proliferation deficits in female APP NL−G−F mice. Estrogen stimulation robustly enhanced BMP6 expression in Neuro2a cells. Conclusions Our findings reveal a sex-dependent impairment of neurogenesis in APP NL−G−F mice driven by BMP signaling. Blocking BMP signaling enhances adult neural stem cell proliferation in female APP NL−G−F mice, providing a potential therapeutic target for AD.