Post-stroke cognitive impairment ( PSCI) is a common and debilitating complication following stroke that involves 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 PSCI onset and recovery. The VN modulates gut microbiota homeostasis, intestinal barrier integrity, and immune responses, indirectly affecting central nervous system inflammation and neural plasticity. Stroke can disrupt VN 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-GBA in PSCI and their interconnected relationships, and explores targeted intervention strategies that may offer promising therapeutic avenues for managing PSCI to contribute to its clinical prevention and treatment.