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Microplastics and Nanoplastics as Potential Contributors to Neurodegenerative Disease: Mechanistic Links to Dementia, Parkinson's Disease, Epilepsy, and Emerging Therapeutic Opportunities
Summary
Researchers reviewed emerging evidence that micro- and nanoplastics may contribute to neurodegeneration by promoting neuroinflammation, oxidative stress, blood-brain barrier disruption, and direct interactions with aggregation-prone proteins like amyloid-β and α-synuclein, proposing that pre-existing neurological disease may increase susceptibility to particulate accumulation in brain tissue.
Microplastics and nanoplastics (MNPs) are increasingly recognized as environmental contaminants with potential neurological relevance. Recent studies reporting particulate material in human brain tissue, including the olfactory bulb, have intensified interest in inhalation and systemic exposure routes to the central nervous system (CNS). Emerging evidence suggests that MNPs may contribute to neurodegenerative pathology through chronic neuroinflammation, oxidative stress, blood-brain barrier (BBB) dysfunction, impaired proteostasis, and direct interactions with aggregation-prone proteins such as amyloid-β, tau, and α-synuclein. These mechanisms may be relevant not only to Alzheimer’s disease and related dementias, but also to Parkinson’s disease and other neurological disorders. This perspective reviews current evidence, proposes a vulnerability framework in which pre-existing neurodegenerative disease may increase susceptibility to particulate accumulation, and outlines therapeutic opportunities including interaction-mediated mitigation, targeted lipid nanoparticle (LNP) delivery, and exposure-responsive biomonitoring.