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This original research article investigates the emerging concept of the vestibular–cognitive axis by exploring the association between genetic variation in the BACE1 rs638405 polymorphism and cognitive vulnerability in patients with vestibular system dysfunction. Alzheimer’s disease (AD) is a leading cause of global cognitive decline, traditionally studied through neurodegenerative and genetic mechanisms. However, growing evidence suggests that sensory system dysfunction, particularly involving the vestibular system, may contribute to cognitive impairment through its connections with hippocampal and cortical networks. In this exploratory case–control study conducted in Batumi, Georgia, a total of 108 participants (vestibular dysfunction, Alzheimer’s disease, and healthy controls) were assessed using standardized neuropsychological instruments and genotyped using TaqMan real-time PCR methods. The study evaluates genotype distribution, cognitive impairment patterns, and potential genetic susceptibility within a clinically relevant framework. The findings indicate a higher frequency of the BACE1 rs638405 GG genotype among patients with vestibular dysfunction compared with controls, suggesting a possible context-dependent genetic signal. Additionally, a substantial proportion of patients with vestibular dysfunction demonstrated measurable cognitive impairment, supporting the hypothesis that vestibular disruption may contribute to cognitive decline. No significant association was observed between the polymorphism and Alzheimer’s disease, highlighting the potential specificity of this genetic signal within vestibular-related cognitive pathways rather than classical neurodegeneration. Given the modest sample size and exploratory design, the results should be interpreted cautiously. Nevertheless, this study contributes to the growing body of evidence supporting the integration of sensory system dysfunction into models of cognitive vulnerability and underscores the need for larger, multi-center studies incorporating comprehensive genetic profiling and longitudinal follow-up. This work is positioned as a hypothesis-generating neurogenetic investigation with implications for understanding individualized cognitive risk and advancing interdisciplinary approaches to neurodegenerative research.