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Nanoplastics exacerbate Parkinson's disease symptoms in C. elegans and human cells
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Researchers discovered that tiny 25-nanometer plastic particles worsened symptoms similar to Parkinson's disease in both worm models and human cells, including nerve cell death, movement problems, and buildup of harmful protein clumps. The nanoplastics also damaged the intestinal barrier, causing a "leaky gut" condition, and broke apart mitochondria in muscle cells. These findings suggest nanoplastic exposure could be a risk factor for neurodegenerative diseases.
The increasing prevalence of nanoplastics in our environment due to the widespread use of plastics poses potential health risks that are not yet fully understood. This study examines the physiological and neurotoxic effects of these minuscule nanoplastic particles on the nematode Caenorhabditis elegans as well as on human cells. Here, we find that 25 nm polystyrene nanoplastic particles can inhibit animal growth and movement at very low concentrations, with varying effects on their surface groups. Furthermore, these nanoplastic particles not only accumulate in the digestive tract but also penetrate further into extraintestinal tissues. Such nanoplastics significantly compromise the integrity of the intestinal barrier, leading to "leaky gut" conditions and cause mitochondrial fragmentation in muscles, which possibly explains the observed movement impairments. A striking discovery was that these nanoplastics exacerbate symptoms similar to those of Parkinson's disease (PD), including dopaminergic neuronal degeneration, locomotor dysfunction, and accumulation of α-Synuclein aggregates. Importantly, our study demonstrates that the detrimental effects of nanoplastics on the aggregation of α-Synuclein extend to both C. elegans and human cell models of PD. In conclusion, our research highlights the potential health hazards linked to the physicochemical properties of nanoplastics, underlining the urgency of understanding their interactions with biological systems. ENVIRONMENTAL IMPLICATION: The escalating prevalence of nanoplastics in the environment due to widespread plastic usage raises potential health risks. Studies conducted on C. elegans indicate that even low concentrations of 25 nm polystyrene nanoplastics can impair growth and movement. These particles accumulate in the digestive system, compromising the intestinal barrier, causing "leaky gut", as well as inducing Parkinson's-like symptoms. Importantly, in both C. elegans and human cell models of Parkinson's disease, such nanoplastics penetrate tissues or cells and increase α-Synuclein aggregates. This underscores the urgent need to understand the interactions of nanoplastics with biological systems and highlights potential environmental and health consequences.
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Environmentally relevant concentrations of polystyrene nanoplastics induce Parkinson’s-like neurotoxicity in C. elegans via oxidative stress
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Researchers exposed roundworms to environmentally realistic concentrations of polystyrene nanoplastics and observed movement problems and brain changes resembling Parkinson's disease. The nanoplastics selectively damaged dopamine-producing neurons and increased toxic protein clumping through oxidative stress, and when an antioxidant treatment was applied, it partially reversed the harmful effects.
PD-like pathogenesis induced by intestinal exposure to microplastics: An in vivo study of animal models to a public health survey
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Researchers found that even low-dose microplastic exposure in mice and worm models accelerated the degeneration of dopamine-producing brain cells and caused movement disorders similar to Parkinson's disease. The microplastics triggered damage through the gut barrier and immune system, causing brain inflammation even without directly entering the brain. A companion public health survey also linked frequent use of disposable plastic tableware to intestinal inflammatory symptoms in people.
Nanoplastics cause an increased risk of Parkinson’s disease compared to microplastics at environmental exposure levels
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Mice that breathed in tiny nanoplastic particles for 16 weeks showed more brain changes linked to Parkinson's disease, such as nerve cell damage and inflammation, than mice exposed to larger microplastic particles. Behavioral problems were also greater in the nanoplastic group, even though the amount reaching the brain was very small.
Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology
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Scientists found that polystyrene nanoplastics can travel from the gut to the brain along nerve pathways and worsen Parkinson's disease in mice. The nanoplastics accelerated the clumping of alpha-synuclein, a protein central to Parkinson's, which triggered brain inflammation, damaged mitochondria, and impaired the cellular cleanup system. Mice exposed to both nanoplastics and the disease protein showed progressive physical and motor decline resembling Parkinson's symptoms.
Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson’s pathology
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Researchers found that oral exposure to polystyrene nanoplastics worsened Parkinson's disease progression in genetically predisposed mice by damaging the gut lining, disrupting the gut microbiome, and altering hundreds of metabolites through the gut-liver axis. The findings suggest that everyday nanoplastic ingestion could accelerate neurodegeneration in people already at risk for Parkinson's disease.
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