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Microglia as a Surrogate Biosensor to Determine Nanoparticle Neurotoxicity
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Analyzing nanoparticle-induced neurotoxicity: A bibliometric analysis.

Xiaomin Wei1, Fuzhen Yang1, Defang Chen1

  • 1Department of Outpatient, Jinan Central Hospital Affiliated to Shandong University, Jinan, Shandong, People's Republic of China.

Toxicology and Industrial Health
|February 26, 2020
PubMed
Summary
This summary is machine-generated.

Nanoparticle exposure may cause unknown health issues. Research shows nanoneurotoxicity is a growing concern, linked to oxidative stress and inflammation in neurodegenerative diseases.

Keywords:
Nanoparticlebibliometric analysisinflammationneurotoxicityoxidative stress

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Area of Science:

  • Environmental Science
  • Biomedical Science
  • Materials Science

Background:

  • Nanoparticles are increasingly used across diverse sectors like cosmetics, agriculture, environment, and biomedicine.
  • This widespread application raises concerns about potential human exposure and associated pathological consequences.

Purpose of the Study:

  • To conduct a bibliometric analysis of research trends in nanoneurotoxicity.
  • To identify key research areas, leading contributors, and prominent publications in the field.

Main Methods:

  • Bibliometric analysis of publications from 2008-2018 using Web of Science Core Collection.
  • Data visualization and analysis performed with CiteSpace and HistCite software.

Main Results:

  • A total of 2932 publications were analyzed, with annual output increasing significantly from 78 to 512 over the decade.
  • The United States (29.5%) and China (22.9%) are leading contributors, with *PLoS One*, *Scientific Reports*, and *Nanoscale* publishing the most articles.
  • Key research themes include nanoneurotoxicity mechanisms such as oxidative stress, inflammation, astrocyte activation, and amyloid-beta protein fibrillation.

Conclusions:

  • Nanoneurotoxicity remains a significant research focus with future potential.
  • Nanoparticles contribute to neurodegenerative diseases via mechanisms including reactive oxygen species generation, inflammation, and altered gene expression/signaling pathways.