Evidence map›Paper›PMID 31818314›Full record

ReviewMolecular brain2019

Zinc transporters in Alzheimer's disease.

Yingshuo Xu, Guiran Xiao, Li Liu, Minglin Lang

Open access · goldAbstract readReview
In one paragraph

Review in Molecular brain, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Reframing Alzheimer's Disease Through a Redox-Metabolic Framework.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. ZIP1 Is a Critical DNA Damage-Responsive Zinc Transporter Induced by Bleomycin via the TNFα-NF-κB Pathway.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Traumatic brain injury-related ferroptosis: current perspectives.Journal of molecular medicine (Berlin, Germany) · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Mechanisms of Cadmium Neurotoxicity.International journal of molecular sciences · 2023
    Review
  16. Review
  17. Article
  18. Review
  19. Article
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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

4 authors at 4 institutions in 1 country.

Yingshuo XuCAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Beijing, 100049, China.
Guiran XiaoSchool of Food and Biological Engineering, Hefei University of Technology, Hefei, 230009, China.
Li LiuState Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Minglin LangCAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Beijing, 100049, China. langml@ucas.ac.cn.ORCID 0000-0003-3801-2675
Chinese Academy of Sciences · CNHebei Agricultural University · CNHefei University of Technology · CNUniversity of Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most devastating neurodegenerative disorder. Due to the increase in population and longevity, incidence will triple by the middle of the twenty-first century. So far, no treatment has prevented or reversed the disease. More than 20 years of multidisciplinary studies have shown that brain zinc dyshomeostasis may play a critical role in AD progression, which provides encouraging clues for metal-targeted therapies in the treatment of AD. Unfortunately, the pilot clinical application of zinc chelator and/or ionophore strategy, such as the use of quinoline-based compounds, namely clioquinol and PBT2, has not yet been successful. The emerging findings revealed a list of key zinc transporters whose mRNA or protein levels were abnormally altered at different stages of AD brains. Furthermore, specifically modulating the expression of some of the zinc transporters in the central nervous system through genetic methods slowed down or prevented AD progression in animal models, resulting in significantly improved cognitive performance, movement, and prolonged lifespan. Although the underlying molecular mechanisms are not yet fully understood, it shed new light on the treatment or prevention of the disease. This review considers recent advances regarding AD, zinc and zinc transporters, recapitulating their relationships in extending our current understanding of the disease amelioration effects of zinc transport proteins as potential therapeutic targets to cure AD, and it may also provide new insights to identify novel therapeutic strategies for ageing and other neurodegenerative diseases, such as Huntington's and Parkinson's disease.

Indexed as

Alzheimer DiseaseAnimalsBrainCarrier ProteinsHomeostasisHumansMolecular Targeted TherapyZincCarrier ProteinsZinczinc-binding proteinAgeingAlzheimer’s diseaseBrainEmerging therapeutic targetGenetic modulationZinc transporter

Identifiers

PMID31818314
PMCPMC6902570
OpenAlexW2994937320

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.