Review synthesizing preclinical evidence that nanoplastics can cross the blood–brain barrier, promote protein aggregation, impair microglial clearance, disrupt the gut–liver–brain axis, and drive neuroinflammation while noting a lack of standardized human exposure data and causal proof.

Although primarily a mechanistic review rather than a translational study, it highlights inflammation, microglial dysfunction, and gut–brain interactions—pathways highly relevant to Parkinson's disease—that could guide biomarker development and targeted preclinical experiments to assess therapeutic…

Nanoplastics are ubiquitous by-products of global plastic production and have emerged as a potentially consequential yet insufficiently defined threat to health. Recent studies have revealed that these synthetic particulates can cross the blood-brain barrier, accelerate amyloid aggregation, impair microglial clearance, hijack the gut-liver-brain axis, and drive neuroinflammation-mechanisms central to neurodegeneration in Alzheimer's and Parkinson's disease. In addition, anionic nanoplastics can induce vascular endothelial leakiness, thereby harboring a paracellular route for their systemic and cerebral access. Yet causality remains unproven in implicating nanoplastics for neurodegeneration in the absence of standardized human exposure data, mechanistic specificity, and epidemiological evidence, especially considering the supra-environmental doses employed. Here, we synthesize current knowledge, examine barriers to causal understanding, and propose a roadmap to advance this emerging scientific frontier of great public concern and inform future strategies for sustainable materials innovation.