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Microplastics and nanoplastics in neurodegenerative disease: A scoping review
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This review of animal and human studies finds that tiny plastic particles may build up in the brain and are linked, in lab animals, to damage resembling Alzheimer's and Parkinson's disease. However, most studies used one lab-made plastic type, not real-world mixtures, so scientists can't yet say microplastics actually cause these diseases in people.
ABSTRACT Plastic pollution has become a global environmental concern, with microplastics and nanoplastics (MNPs) increasingly detected in human tissues, including the brain. This scoping review conducted in accordance with the SYRCLE and ROBINS-I Risk of Bias tool methodology and reported following the PRISMA extension for Scoping Reviews (PRISMA-ScR), synthesized current evidence on the potential association between MNP exposure and neurodegenerative diseases, particularly Alzheimer’s disease (AD) and Parkinson’s disease (PD). Following PRISMA guidelines, systematic searches identified 93 records and 13 eligible studies with two involving human subjects and eleven preclinical. Human data provide preliminary evidence that MNPs may be present in brain tissue, although recent methodological critiques have questioned the reliability of current detection methods in lipid-rich tissues. Preclinical studies provide more consistent mechanistic evidence. MNP exposure, predominantly polystyrene, was associated with oxidative stress, neuroinflammation, mitochondrial dysfunction, impaired autophagy, and neuronal apoptosis. In AD models, MNP exposure exacerbated tau phosphorylation, amyloid-β aggregation, and cognitive decline. In PD models, MNPs accelerated α-synuclein aggregation and dopaminergic neuron loss, and motor impairment through mechanisms including excessive mitophagy autophagosomelysosome disruption, and mitochondrial calcium dysregulation. Biodegradable polymers such as polylactic acid also demonstrated neurotoxic potential. The overwhelming reliance on polystyrene in experimental studies does not reflect actual environmental polymer distributions. Formal quality assessment revealed unclear risk of bias in several domains across preclinical studies. Accordingly, a causal relationship between MNP exposure and neurodegenerative disease has not yet been established. Further longitudinal studies using environmentally relevant exposures and validated analytical methods are needed to determine whether MNPs pose a genuine risk to neurological health.
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