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Nanoplastics-induced neurotoxicity: neurovascular dysfunction, cognitive impairment, and mechanisms of cell death.
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This review summarizes existing research on how tiny plastic particles called nanoplastics may affect the brain. Studies in lab models suggest these particles can disrupt the brain's protective barrier, trigger cell stress and death, and interfere with brain cell communication, which researchers link to memory and behavior problems in experimental models.
Nanoplastics (NPs) are increasingly recognized as environmentally persistent contaminants capable of reaching the central nervous system (CNS), yet the mechanistic basis linking brain exposure to cognitive dysfunction remains incompletely resolved. Emerging evidence indicates that NPs can cross or perturb the blood-brain barrier (BBB), accumulate within neural tissues, and interact with neurons, microglia, astrocytes, neural progenitors, and cerebrovascular cells. These interactions have been associated with oxidative stress, mitochondrial dysfunction, neuroinflammation, synaptic injury, and disruption of hippocampal homeostasis, although the strength and causal nature of evidence for individual mechanisms vary across experimental models. Importantly, regulated cell death (RCD) is emerging as a critical mechanistic bridge between cellular toxicity and neurocognitive outcomes, encompassing apoptosis, pyroptosis, ferroptosis, and cuproptosis. However, evidence for specific cell-death pathways remains largely based on molecular and cellular signatures in experimental models, and oxidative stress, mitochondrial dysfunction, or altered expression of pathway-associated proteins alone should not be considered definitive evidence of pathway activation. Recent studies further implicate microglial extracellular traps, excessive mitochondrial fission, and glymphatic dysfunction as potentially important pathways connecting NP exposure with neuronal injury and cognitive decline. Environmental co-exposures may intensify these effects, highlighting the context-dependent nature of NP neurotoxicity. This review integrates current evidence linking NP exposure to cognitive and behavioral abnormalities, emphasizing the interconnected roles of neurovascular dysfunction, glial-neuronal crosstalk, oxidative-mitochondrial stress, synaptic disruption, RCD, and impaired brain clearance mechanisms.
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Brain under siege: the role of micro and nanoplastics in neuroinflammation and oxidative stress
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This review examines emerging evidence that micro- and nanoplastics can cross the blood-brain barrier and accumulate in nervous tissue, potentially triggering neuroinflammation and oxidative stress. Researchers summarized findings showing these particles may act as neurotoxicants that contribute to synaptic dysfunction and pathological changes in brain cells. The study highlights the need for further research into how chronic plastic particle exposure may affect central nervous system health over time.
Deciphering the Neurotoxic Burden of Micro- and Nanoplastics: From Multi-model Experimental Evidence to Therapeutic Innovation
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This review summarizes research on how micro- and nanoplastics damage the brain and nervous system, covering evidence from cell studies, animal experiments, and clinical observations. Plastic particles can cross the blood-brain barrier, disrupt the gut-brain connection, cause oxidative stress, and trigger inflammation that leads to memory problems and cognitive decline. The review also discusses potential treatment strategies, making it a useful resource for understanding the brain health risks of plastic exposure.
Microplastics/nanoplastics and neurological health: An overview of neurological defects and mechanisms
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This review summarizes evidence that micro and nanoplastics can harm the nervous system, causing developmental abnormalities, brain cell death, neurological inflammation, and potentially contributing to neurodegenerative diseases. Animal studies show that these tiny plastics can cross the blood-brain barrier and accumulate in brain tissue, where they trigger oxidative stress and disrupt normal brain function. While direct evidence in humans is still limited, the findings suggest that chronic microplastic exposure could be a risk factor for neurological health problems.
From exposure to neurotoxicity induced by micro-nanoplastics with brain accumulation and cognitive decline
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This review synthesizes evidence that micro- and nanoplastics can reach the brain by crossing the blood-brain barrier or traveling along nerve pathways, accumulating in regions critical for memory and thinking. Animal studies show that chronic exposure leads to cognitive problems, behavioral changes, and brain changes resembling neurodegenerative diseases, driven by oxidative stress, inflammation, and disruption of the gut-brain connection. The findings raise concern that long-term human exposure to nanoplastics through food and air could contribute to cognitive decline and neurological disease.
Mechanisms of micro- and nanoplastics on blood-brain barrier crossing and neurotoxicity: Current evidence and future perspectives
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This review examines evidence that micro- and nanoplastics can cross the blood-brain barrier, the protective shield around the brain, through multiple pathways including disrupting the barrier's tight junctions and being transported inside cells. Once in the brain, these particles may cause damage through oxidative stress, inflammation, mitochondrial dysfunction, and disrupted iron metabolism, with effects worsened when plastics carry other pollutants like heavy metals.
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