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Lifelong exposure to polystyrene-nanoplastics induces an attention-deficit hyperactivity disorder-like phenotype and impairs brain aging in mice
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Mice exposed to nanoplastics throughout their entire lives -- from the womb through old age -- developed ADHD-like symptoms as adults, including hyperactivity, risk-taking behavior, and impaired learning, and showed a lower seizure threshold in old age. These behavioral changes were accompanied by altered brain proteins and accelerated brain aging at the cellular level, suggesting lifelong nanoplastic exposure may contribute to neurodevelopmental and neurodegenerative disorders.
The accumulation of plastic waste in the environment, breaking down into micro- and nanoplastics, poses significant threats to ecosystem and human health. Plastic particles have been detected in human blood, urine, and placental tissue, indicating widespread exposure. While their long-term health impacts remain unclear, developing brains, especially in fetuses and children, may be vulnerable, potentially resulting in behavioral changes or neurodevelopmental disorders. This study explores the effects of chronic exposure to 23-nm polystyrene nanoplastics at 10 µg/day/kg in wild-type mice across life stages, using exposure levels reflective of human reality. Maternal exposure disrupted critical developmental milestones in pups. In adulthood, exposed mice exhibited Attention-Deficit Hyperactivity Disorder (ADHD)-like traits, including hyperactivity, increased risk-taking behaviors, and impaired motor learning and executive functions. In aging mice, exposure was associated with a lower epileptic threshold, with developing seizures. These behavioral changes were linked to altered gene and synaptic protein expression associated with ADHD and epilepsy. At the cellular level, lifelong nanoplastic exposure caused lysosomal dysfunctions and increased lipofuscin accumulation, indicative of accelerated brain aging. These findings align with the growing prevalence of ADHD and epilepsy in humans, particularly children and the elderly, emphasizing the urgent need to address plastic pollution and its health implications.
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Short-term PS-NP exposure in early adulthood induces neuronal damage in middle-aged mice via microglia-mediated neuroinflammation
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Researchers orally dosed young mice with polystyrene nanoplastics for one week and observed, ten months later, that particles persisted in brain tissue and drove microglial-mediated neuroinflammation, synapse loss, and cognitive impairment — with minocycline treatment confirming that microglial activation was the key driver of long-term neuronal damage.
Cerebral to SystemicRepresentations of Alzheimer’sPathogenesis Stimulated by Polystyrene Nanoplastics
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Researchers exposed both wild-type and APP/PS1 Alzheimer's model mice to environmental levels of polystyrene nanoplastics and measured Alzheimer's-like pathology progression. Nanoplastics exacerbated cognitive decline, microglial activation, and hippocampal neuronal death, particularly in the Alzheimer's model, with systemic inflammatory effects suggesting plastic particles may accelerate neurodegeneration.
Adolescent exposure to micro/nanoplastics induces cognitive impairments in mice with neuronal morphological damage and multi-omic alterations
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Adolescent mice exposed to polystyrene nanoplastics showed significant memory and learning problems, along with neuron loss and reduced new brain cell growth in the hippocampus. The nanoplastics also disrupted gut bacteria and brain chemistry, with strong links found between gut microbiome changes and brain metabolic disruption, suggesting that plastic exposure during youth may impair brain development through the gut-brain connection.
Cerebral to Systemic Representations of Alzheimer’s Pathogenesis Stimulated by Polystyrene Nanoplastics
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Researchers found that environmentally realistic levels of polystyrene nanoplastics worsened Alzheimer's disease symptoms in mice, triggering brain inflammation, neuron death, and cognitive decline. The nanoplastics also disrupted metabolism and caused organ damage beyond the brain, including liver and kidney effects. This study provides some of the first evidence that nanoplastic exposure could accelerate brain diseases like Alzheimer's, especially as nanoplastics have been found in human brain tissue.
Teratological, neurochemical and histomorphic changes in the limbic areas of F1 mice progeny due to co-parental polystyrene nanoplastic exposure
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Researchers exposed parent mice to polystyrene nanoplastics before and during pregnancy and found that offspring exhibited skeletal and visceral malformations, impaired neonatal reflexes, learning deficits, and structural brain changes — including reduced hippocampal neurons — demonstrating transgenerational neurodevelopmental harm from nanoplastic exposure.
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