Evidence map›Paper›PMID 38206494›Full record

ReviewBiological trace element research2024

Inflammation in Metal-Induced Neurological Disorders and Neurodegenerative Diseases.

Ruokun Wei, Peiqi Wei, Haiyan Yuan, Xiang Yi, Michael Aschner, Yue-Ming Jiang, Shao-Jun Li

Abstract readReview
PubMed Publisher
In one paragraph

Review in Biological trace element research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–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

15 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Application of Modulators of CaInternational journal of molecular sciences · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
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

7 authors.

Ruokun Wei *Toxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China.
Peiqi Wei *Toxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China.
Haiyan Yuan *Toxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China.
Xiang YiToxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China.
Michael AschnerThe Department of Molecular Pharmacology at Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Yue-Ming JiangToxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China. ymjianggxmu@163.com.
Shao-Jun LiToxicology Department, School of Public Health, Guangxi Medical University, 22 Shuang-yong Rd., Nanning, 530021, China. lishaojun0613@163.com.

Funding

Guangxi Natural Science Foundation 2018GXNSFBA050060National Natural Science Foundation of China NSFC82160626
6 · The paper itself

Abstract

Essential metals play critical roles in maintaining human health as they participate in various physiological activities. Nonetheless, both excessive accumulation and deficiency of these metals may result in neurotoxicity secondary to neuroinflammation and the activation of microglia and astrocytes. Activation of these cells can promote the release of pro-inflammatory cytokines. It is well known that neuroinflammation plays a critical role in metal-induced neurotoxicity as well as the development of neurological disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Initially seen as a defense mechanism, persistent inflammatory responses are now considered harmful. Astrocytes and microglia are key regulators of neuroinflammation in the central nervous system, and their excessive activation may induce sustained neuroinflammation. Therefore, in this review, we aim to emphasize the important role and molecular mechanisms underlying metal-induced neurotoxicity. Our objective is to raise the awareness on metal-induced neuroinflammation in neurological disorders. However, it is not only just neuroinflammation that different metals could induce; they can also cause harm to the nervous system through oxidative stress, apoptosis, and autophagy, to name a few. The primary pathophysiological mechanism by which these metals induce neurological disorders remains to be determined. In addition, given the various pathways through which individuals are exposed to metals, it is necessary to also consider the effects of co-exposure to multiple metals on neurological disorders.

Indexed as

InflammationMetalsNeurodegenerative DiseasesAnimalsHumansMicrogliaNervous System DiseasesNeuroinflammatory DiseasesOxidative StressMetalsMetalsNeurodegenerative diseaseNeuroinflammationNeurological disorders

Identifiers

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.