Post-stroke cognitive impairment (PSCI) is a common and debilitating complication following stroke,involving complex mechanisms such as neuroinflammation,neurotransmitter imbalance, and impaired neural plasticity. Recently,the vagus nerve (VN)-mediated gut-brain axis (GBA), a vital bidirectional communication pathway between the central nervous system and the gut, has gained increasing attention for its pivotal role in the onset and recovery of PSCI. The vagus nerve modulates gut microbiota homeostasis, intestinal barrier integrity, and immune responses, thereby indirectly affecting central nervous system inflammation and neural plasticity. Stroke can disrupt vagal signaling, resulting in gut microbiota dysbiosis and altered metabolite production, which further trigger central inflammatory responses and worsen cognitive dysfunction. This review synthesizes current evidence on the mechanisms of the VN-mediated gut-brain axis (VN-GBA) in PSCI and their interconnected relationships, and explores targeted intervention strategies that may offer promising therapeutic avenues for managing post-stroke cognitive impairment. These insights aim to contribute to the clinical prevention and treatment of PSCI.