Objective To investigate the effects of fecal microbiota transplantation（FMT） on the cognitive ability，microbiota composition，metabolites，and inflammatory response of mice with delayed neurocognitive recovery（dNCR），and to provide insights into the development of effective treatments for dNCR patients. Methods Mice were randomly divided into the control group，model group，and FMT group. The dNCR model was established by middle tibial fracture，and fecal samples were collected from healthy mice for FMT. Cognitive ability was assessed using the Morris water maze test（MWMT） and open field test（OFT）. IL-6，IL-1β and TNF-α levels in the hippocampus and serum were measured using ELISA. Colonic Z0-1 and hippocampal NSE and S-100β protein expression was measured by Western blot. The microbiota composition and changes in metabolites were examined using 16s rRNA sequencing and LC-MS，respectively. Results OFT and MWMT showed that model mice had cognitive impairment，which was attenuated in FMT mice. Serum and hippocampal levels of IL-6，IL-β and TNF-α were higher in the model group than in the other two groups. In addition，the model group had significantly lower colonic ZO-1 protein expression（P=0.000） but significantly higher hippocampal NSE and S-100β protein expression than the other two groups（P=0.000）. The Chao1 index and Shannon index were similar among the three groups. Principle coordinates analysis using Bray-Curtis dissimilarity revealed that the microbiota composition of model group was markedly distinct from those of the control and FMT groups. Bacteroidetes and Firmicutes were the predominant phyla in the model and FMT groups. The model group also had higher abundance of Firmicutes，Desulfobacterota，and Proteobacteria and lower abundance of Bacteroides than the control group and FMT group. Partial least-squares discriminant analysis demonstrated that the model group had a distinct metabolite composition than the other two groups，characterized by decreased tryptophan，5-hydroxytryptophan，and indole，as well as increased lysophosphatidylcholine. Conclusion Dysregulated microbiota and metabolites as well as inflammatory responses may be the key mechanisms driving dNCR development and progression. FMT can act on these pathways to improve the cognitive function of anesthetized or operated mice.