Objective To investigate the effects of electroacupuncture （EA） at “Baihui （GV 20），”“Pishu （BL 20），” and “Zusanli （ST 36）” on the learning and memory functions of rats with Alzheimer′s disease （AD） induced by Aβ1?42. Additionally， the mechanism of EA in treating AD was explored from the perspective of the inflammatory cascade mediated by the NF?κB/NLRP3/Caspase?1 signaling pathway. Methods A rat model of Alzheimer′s disease was established by bilateral injection of Aβ1?42 solution into the C1 region of the hippocampus. According to the random number table method， 32 male SPF?grade rats were divided into four groups （n = 8 per group）： a sham?operated group， a model group， an electroacupuncture （EA） group， and a Western medicine group （donepezil hydrochloride）. The EA group received electroacupuncture at the “Baihui”， “Pishu”， and “Zusanli” acupoints； the Western medicine group received donepezil hydrochloride via gavage. After the treatment period， Morris water maze experiments were conducted to evaluate learning and memory abilities. Hematoxylin and eosin （HE） staining was used to examine morphological changes in hippocampal tissues. Enzyme?linked immunosorbent assay （ELISA） was employed to measure serum levels of TNF?α and IL?1β. Western blotting and immunofluorescence staining were utilized to assess the co?expression levels of NF?κB p65， NLRP3， and Caspase?1 proteins in the hippocampal region. Results Compared with the sham?operated group， rats in the post?modeling group exhibited significantly prolonged escape latency （P < 0.05）， reduced crossings of the original platform location， and decreased time spent in the target quadrant （P < 0.05）. Additionally， nuclear morphology was altered， neurons surrounding the hippocampus displayed necrosis， vacuolar degeneration， and chromatin marginalization. Serum levels of TNF?α and IL?1β were elevated （P < 0.05）， and protein expression levels as well as fluorescent positivity for NF?κB p65， NLRP3， and caspase?1 in the hippocampus were increased （P < 0.05）. Compared with the model group， rats in both the EA and Western medicine groups showed a trend toward shorter escape latency （P < 0.05）， increased crossings of the original platform location and time spent in the target quadrant （P < 0.05）. Cell structures were largely intact， with only a few nuclei showing slight irregularities and some chromatin accumulation at the edges. Serum levels of TNF?α and IL?1β were reduced （P < 0.05）， and protein expression levels and fluorescence positivity for NF?κB p65， NLRP3， and caspase?1 in the hippocampus were also decreased （P < 0.05）. Conclusion EA enhances the learning and memory capabilities of AD rats， potentially by downregulating the NF?κB/NLRP3/Caspase?1 + signaling + pathway and decreasing the release of neuroinflammatory factors， thereby alleviating cognitive dysfunction in AD rats.