Objective To investigate the effects of Bushen Jianpi Kaixin formula (BSJPKXF) on the learning and memory abilities of Alzheimer’s disease (AD) model rats, the related autophagy and apoptosis in their cortex, and the underlying mechanism of BSJPKXF. Methods Sixty rats were randomly divided into six groups (n=10): control group, AD group, Bushen group (BS, 3. 6 g/ (kg·d)), Jianpi group (JP, 4. 05 g/ (kg·d)), Kaixin group (KX, 2. 34 g/ (kg·d)), and Bushen Jianpi Kaixin group (BSJPKXF, 9. 99 g/ (kg·d)). The AD model was established by intraperitoneal injection of D-gal. Rats in BS, JP, KX and BSJPKXF groups were gavaged with corresponding drugs once a day. Rats in control and AD groups were treated with an equal volume of normal saline once per day. After 4 weeks, learning and memory abilities were assessed by the Morris water maze. The open-field test was used to assess cognitive functions. LC3-I, LC3-II and Beclin1 expression in cerebral cortical tissues was detected by Western blot. Bax and Bcl-2 expression in cerebral cortical tissues was detected by immunohistochemistry. Beclin1, P62, Bax and Bcl-2 mRNA expression in cerebral cortical tissues was detected by RT-PCR. Results Compared with the control group, D-gal significantly decreased the spatial learning and memory abilities in the AD group (P<0. 01), decreased Beclin1, LC3-I/ LC3-II and Bcl-2 expression and the Bcl-2/ Bax ratio, and increased P62 and Bax mRNA expression (P<0. 01). After treatment, compared with the AD model group, Bushen Jianpi Kaixin formula improved the spatial learning memory ability in the BSJPKXF group (P<0. 01), increased Beclin1, LC3-I/ LC3-II and Bcl-2 expression and the Bcl-2/ Bax ratio, and decreased P62 and Bax mRNA expression (P<0. 01). Conclusions Bushen Jianpi Kaixin formula improved cognitive impairment in AD rats. The mechanism was presumed related to the reduction of neural autophagy and apoptosis.