From the Gut to the Brain: Microplastic‐Associated Neurovascular Dysfunction and Implications for Stroke Risk

Jan 12, 2026Advanced science (Weinheim, Baden-Wurttemberg, Germany)

Microplastics from the Gut Linked to Brain Blood Vessel Problems and Higher Stroke Risk

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Gut-Brain Axis on OpenScience ↗PubMed ↗DOI ↗OA ↗

Abstract

Microplastics (MPs) may disrupt gut microbial balance and impair intestinal barrier function.

Accumulating evidence indicates that MPs can engage the gut-brain axis, leading to systemic inflammation.
Disruption of gut health is associated with blood-brain barrier dysfunction and neurovascular changes.
Animal and in vitro models suggest that MP exposure could increase susceptibility to strokes.
Findings highlight potential mechanisms such as endothelial inflammation and atherosclerosis linked to MP exposure.
Variability in exposure conditions complicates direct causal connections in human studies.
Future research should focus on standardized methods and advanced analytical techniques to clarify these relationships.

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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.