Evidence map›Paper›PMID 41306300›Full record

ArticleEnvironment & health (Washington, D.C.)2025

Cerebral to Systemic Representations of Alzheimer's Pathogenesis Stimulated by Polystyrene Nanoplastics.

Yue Wang, Xiufang Liang, Nicholas Andrikopoulos, Shufang Zheng, Yuhuan Li, Pu Chun Ke

Abstract read
In one paragraph

Article in Environment & health (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Nanoplastics and Neurodegeneration: A Roadmap From Mechanism to Causation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Yue WangSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou 510006, China.
Xiufang LiangSchool of Biomedical Sciences and Engineering, Guangzhou International Campus, South China University of Technology, Guangzhou 510006, China.
Nicholas AndrikopoulosDrug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville, Victoria 3052, Australia.
Shufang ZhengSchool of Public Health, Health Science Center, Ningbo University, Ningbo 315211, China.
Yuhuan LiDrug Delivery, Disposition and Dynamics, Monash Institute of Pharmaceutical Sciences, Monash University, 381 Royal Parade, Parkville, Victoria 3052, Australia.
Pu Chun KeNanomedicine Center, The Great Bay Area National Institute for Nanotechnology Innovation, 136 Kaiyuan Avenue, Guangzhou 510700, China.ORCID https://orcid.org/0000-0003-2134-0859

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plastics discharged into the ecosphere can transform into micro- and nanoparticles to instigate interactions with biosystems, posing a threat to environmental sustainability and human health. While nanoplastics have recently been identified in abundance in the human brain, especially in the decedent brain tissues of dementia subjects, how these exogenous miniatures mediate neurological as well as systemic pathologies remains unclear. Here, we first investigated how environmental-level nanoplastic exposure influences the progression of Alzheimer's disease, from cerebral to systemic representations. Specifically, polystyrene nanoplastics aggravated Alzheimer's-like symptoms in both wild-type and APP/PS1 mice and stimulated microglial activation and hippocampal neuronal death, accentuated by peripheral abnormalities of lipid accumulation, hepatic steatosis, inflammation, adipocyte enlargement, and gut microbiota imbalance. These findings implicate that nanoplastic-induced neurological damage is not confined within the brain but expands systemically through the gut-liver-brain axis, thereby contributing to the multiscale and multidirectional progression of Alzheimer's pathophysiology.

Indexed as

Alzheimer’s diseaseamyloid betamicrogliananoplasticssystemic

Identifiers

PMID41306300
PMCPMC12645312

What OpenQuestion holds

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Registered trials

None linked

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.