ArticleCells2025
Effects of Microplastic Accumulation on Neuronal Death After Global Cerebral Ischemia.
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular and Cellular Effects of Microplastics and Nanoplastics in the Pathogenesis of Cardiovascular, Nervous, Urinary, Digestive, and Reproductive System Diseases: A Global Systematic Review.International journal of molecular sciences · 2025Pooled it
- Microplastics as Emerging Neurotoxins: Brain Accumulation, Neuroinflammation, and Neurodegeneration Risk.Journal of biochemical and molecular toxicology · 2026Review
- Micro- and Nanoplastics as a Potential Risk Factor for Stroke: A Systematic Review.Journal of xenobiotics · 2026Review
- Do microplastics play a role in the pathogenesis of neurodegenerative diseases? Shared pathophysiological pathways for Alzheimer's and Parkinson's disease.Molecular and cellular biochemistry · 2026Review
- From the Gut to the Brain: Microplastic-Associated Neurovascular Dysfunction and Implications for Stroke Risk.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The Plastic Within: Micro- and Nanoplastics in Human Tissues and the Nutritional Context for Exposure Mitigation.Nutrition and metabolic insights · 2026Review
- Prenatal exposure to polystyrene nanoparticles induces neuroimmune dysregulation in the adult mouse brain.Zoological research · 2025Article
- Time-dependent expression of neural oxidative and inflammatory biomarkers in ischemic stroke using a transient MCAO rat model.Scientific reports · 2025Article
- Nano- and Microplastics in the Brain: An Emerging Threat to Neural Health.Nanomaterials (Basel, Switzerland) · 2025Review
- Risk Assessment of Microplastics in Humans: Distribution, Exposure, and Toxicological Effects.Polymers · 2025Review
- An overview of research on the association between microplastics and central nervous system disorders.Frontiers in public health · 2025Review
- Overall effects of microplastics on brain.Frontiers in toxicology · 2025Review
- A novel risk factor for dementia: chronic microplastic exposure.Frontiers in neurology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Brain ischemia, a condition in which the brain is deprived of blood flow, can lead to a stroke due to blocked or unstable blood vessels. Global cerebral ischemia (GCI), characterized by an interruption in blood flow, deprives the brain of oxygen and nutrients, producing reactive oxygen species (ROS) that trigger cell death, which kills nerve cells. Microplastics (MPs), tiny environmental pollutants, can enter the human body through contaminated food, water, disposable items, cosmetics, and more. Once in the brain, MPs can increase neuroinflammation by overstimulating inflammatory factors such as microglia. MPs can also damage neurons by scratching myelin and microtubules, slowing signal transduction, causing cognitive impairment, and leading to neuronal death. Furthermore, microtubule damage may result in the release of phosphorylated tau proteins, potentially linked to Alzheimer's disease. We hypothesized that MPs could exacerbate neuroinflammation and microtubule destruction after GCI, leading to increased neuronal death. To test this hypothesis, we administered MPs (0.5 µm) orally at a dose of 50 mg/kg before and after inducing GCI. Staining techniques such as Fluoro-Jade B (FJB), ionized calcium-binding adaptor molecule 1 (Iba-1), cluster of differentiation 68 (CD68), myelin basic protein (MBP), and microtubule-associated protein 2 (MAP2) were used, along with Western blot analysis for interleukin-6 (IL-6), TNF-α, tau-5, and phospho-tau (S396) to evaluate the effects of MPs on neuronal cell death, neuroinflammation, and microtubule destruction. The results showed that MP accumulation significantly increased neuroinflammation, microtubule disruption, and neuronal cell death in the GCI-MP group compared to the GCI-vehicle group. Therefore, this study suggests that MP accumulation in daily life may contribute to the exacerbation of the disease, potentially leading to severe neuronal cell death after GCI.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.