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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 review how microplastics and nanoplastics may reach the brain via inhalation and systemic routes, proposing that chronic neuroinflammation, oxidative stress, and direct interactions with proteins like amyloid-β and α-synuclein could link particle exposure to Alzheimer's, Parkinson's, and other neurodegenerative conditions.
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.