To explore the mechanism of electroacupuncture in improving the cognitive function of amyloid precursor protein(APP)/presenilin 1(PS1) transgenic mice from the perspective of neuroinflammation.Methods:Forty APP/PS1 transgenic mice were randomly divided into model group，electroacupuncture group，western medicine group and electroacupuncture+western medicine group，with 10 in each group.Another 10 C57BL/6 wild rats were taken as the blank group.Electroacupuncture group was stimulated by acupuncture at Baihui(GV 20) and bilateral Shenshu(BL 23).Western medicine group was treated with donepezil solution by gavage.Electroacupuncture+western medicine group received acupuncture stimulation as well as donepezil solution by gavage.Blank group and model group were given distilled water by gavage.After 28 days of intervention，Morris water maze test was performed to detect the escape latency，time spending in target quadrant，and number of crossing platforms of mice in each group.Hematoxylin-eosin staining was used to observe the pathological changes of frontal lobe neurons.Western blot was used to detect the expressions of tumor necrosis factor-α(TNF-α) and nuclear factor-kappa B(NF-κB) in frontal lobe tissues of mice in each group.Results:Morris water maze test revealed that electroacupuncture group，western medicine group and electroacupuncture+western medicine group had decreased escape latency，prolonged time spending in target quadrant，and increased number of crossing platforms(P<0.05).HE staining indicated that compared with conditions in model group，the number and morphology of frontal lobe neurons in electroacupuncture group，western medicine group and electroacupuncture+western medicine group were improved.Western blot found a decrease in the contents of TNF-α and NF-κB in electroacupuncture group，western medicine group and electroacupuncture+western medicine group as compared with those in model group(P<0.05).Conclusion:Electroacupuncture can improve the cognitive function of Alzheimer's disease mice by inhibiting the release of TNF-α and NF-κB，and reducing neuroinflammation and neuronal apoptosis in frontal cortex.