Abstract
Microplastics (MPs) have emerged as pervasive environmental contaminants with increasing relevance to neurovascular health. Following oral exposure, accumulating evidence suggests that MPs can disrupt gut microbial homeostasis, impair intestinal epithelial barrier integrity, and engage the gut-brain axis (GBA), thereby promoting systemic and central inflammatory responses. These interconnected processes are linked to blood-brain barrier (BBB) dysfunction, cerebral microvascular impairment, and neurovascular alterations that are biologically relevant to stroke susceptibility. Evidence derived largely from animal and in vitro models, together with emerging epidemiological observations, supports the biological plausibility that microplastic (MP) exposure may contribute to neurovascular vulnerability through mechanisms involving endothelial inflammation, pro-thrombotic signaling, and atherosclerotic progression. However, substantial heterogeneity in exposure paradigms, particle characteristics, and analytical methodologies limits direct causal inference and translational interpretation in humans. Future research should prioritize standardized exposure frameworks and integrate multi-omics approaches with artificial intelligence (AI)-assisted analysis to better define exposure-response relationships and mechanistic pathways underlying MP-associated cerebrovascular alterations. Such efforts are essential for improving risk assessment and informing evidence-based strategies for environmental neurovascular health.