0
Article Tier 2 Human Health Effects Nanoplastics Sign in to save

Dysfunctional digestive tract highlights the metabolic hallmarks of nanoplastic-exacerbated Parkinson’s pathology

AI summary Read the abstract

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.

Parkinson's disease (PD) is increasingly viewed as both a neurological and metabolic disorder, with the gut-brain axis playing a key role. This study explored how polystyrene (PS) nanoplastics contributed to PD progression by examining their metabolic impact in an A53T α-synuclein (αS) mouse model. Mice given PS nanoplastics orally (2 mg/kg every other day for three months) displayed compromised gut barrier integrity, including a 30% drop in goblet cells and increased epithelial apoptosis in the ileum. Microbial diversity in the ileum rose sharply, with an overgrowth of Desulfovibrio spp. linked to neuroinflammation and αS aggregation. KEGG analysis confirmed apoptosis and lipopolysaccharide biosynthesis pathways influenced by nanoplastics, while metabolomics identified over 200 altered fecal metabolites, including those associated with cytochrome P450 activity and disruptions to cancer-related pathways. Additionally, histopathology revealed liver inflammation, underscoring the systemic effects of nanoplastic exposure. Overall, our findings suggest that environmental nanoplastics may aggravate PD physiopathology through gut-liver axis disruption and metabolic dysregulation.

More Papers Like This

Article Tier 2

Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology

AI summary Read the abstract

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.

Article Tier 2

PD-like pathogenesis induced by intestinal exposure to microplastics: An in vivo study of animal models to a public health survey

AI summary Read the abstract

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.

Article Tier 2

Intergenerational neurotoxicity of polystyrene nanoplastics in offspring mice is mediated by dysfunctional microbe-gut-brain axis

AI summary Read the abstract

Researchers found that mother mice exposed to polystyrene nanoplastics during pregnancy and nursing passed neurological harm to their offspring, with the babies showing brain inflammation, disrupted dopamine and serotonin signaling, and gut microbiome imbalances — suggesting that nanoplastic exposure before birth can damage the developing brain through the gut-brain connection.

Article Tier 2

Nano‐plastics disrupt systemic metabolism by remodeling the bile acid–microbiota axis and driving hepatic–intestinal dysfunction

AI summary Read the abstract

Mice were exposed to polyethylene terephthalate nanoparticles, and researchers used histopathology, metabolomics, and metagenomics to track downstream effects. Nanoplastic ingestion caused severe metabolic disruption—including weight loss, organ atrophy, and liver-intestinal dysfunction—by remodeling the bile acid–gut microbiota axis.

Article Tier 2

Brain single-nucleus transcriptomics highlights that polystyrene nanoplastics potentially induce Parkinson’s disease-like neurodegeneration by causing energy metabolism disorders in mice

AI summary Read the abstract

In a mouse study, oral exposure to polystyrene nanoplastics caused brain changes resembling Parkinson's disease, including loss of dopamine-producing neurons and movement problems. Advanced single-cell brain analysis revealed that the nanoplastics disrupted energy production in brain cells, particularly in the brain regions most affected by Parkinson's disease. This research raises the alarming possibility that chronic nanoplastic exposure through food and water could contribute to neurodegenerative diseases.

Research digests by email

When a large batch of papers lands in the Atlas, we read through it and send a short write-up of what stood out.

Email me about

Share this paper