Evidence map›Paper›PMID 33081348›Full record

ReviewInternational journal of molecular sciences2020

Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.

Hafza Wajeeha Ejaz, Wei Wang, Minglin Lang

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 3 pooled it
8.3field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 3 syntheses or guidelines pooled it, 135 citations in OpenAlex.

  1. Pooled it
  2. Meta-Analysis of Transcriptomic Studies of Blood and Six Brain Regions Identifies a Consensus of 15 Cross-Tissue Mechanisms in Alzheimer's Disease and Suggests an Origin of Cross-Study Heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2025
    Pooled it
  3. Pooled it
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Evaluation of a New Methylimidazole-Containing Thiosemicarbazone as a CuChemistry (Weinheim an der Bergstrasse, Germany) · 2026
    Article
  11. Article
  12. Article
  13. Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025
    Review
  14. Article
  15. 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

3 authors at 3 institutions in 2 countries.

Hafza Wajeeha EjazCAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Yuquan Road 19, Beijing 100049, China.
Wei WangSchool of Medical and Health Sciences, Edith Cowan University, Perth WA6027, Australia.ORCID 0000-0002-1430-1360
Minglin LangCAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Yuquan Road 19, Beijing 100049, China.ORCID 0000-0003-3801-2675
Edith Cowan University · AUHebei Agricultural University · CNUniversity of Chinese Academy of Sciences · CN

Funding

National Natural Science Foundation of China 31571042
6 · The paper itself

Abstract

Alzheimer's disease (AD) is an irreversible, age-related progressive neurological disorder, and the most common type of dementia in aged people. Neuropathological lesions of AD are neurofibrillary tangles (NFTs), and senile plaques comprise the accumulated amyloid-beta (Aβ), loaded with metal ions including Cu, Fe, or Zn. Some reports have identified metal dyshomeostasis as a neurotoxic factor of AD, among which Cu ions seem to be a central cationic metal in the formation of plaque and soluble oligomers, and have an essential role in the AD pathology. Cu-Aβ complex catalyzes the generation of reactive oxygen species (ROS) and results in oxidative damage. Several studies have indicated that oxidative stress plays a crucial role in the pathogenesis of AD. The connection of copper levels in AD is still ambiguous, as some researches indicate a Cu deficiency, while others show its higher content in AD, and therefore there is a need to increase and decrease its levels in animal models, respectively, to study which one is the cause. For more than twenty years, many in vitro studies have been devoted to identifying metals' roles in Aβ accumulation, oxidative damage, and neurotoxicity. Towards the end, a short review of the modern therapeutic approach in chelation therapy, with the main focus on Cu ions, is discussed. Despite the lack of strong proofs of clinical advantage so far, the conjecture that using a therapeutic metal chelator is an effective strategy for AD remains popular. However, some recent reports of genetic-regulating copper transporters in AD models have shed light on treating this refractory disease. This review aims to succinctly present a better understanding of Cu ions' current status in several AD features, and some conflicting reports are present herein.

Indexed as

Alzheimer DiseaseAnimalsChelating AgentsChelation TherapyCopperHumansChelating AgentsCopperAlzheimer’s diseaseamyloid plaquescopperneurodegenerationoxidative damagesprotein modification

Identifiers

PMID33081348
PMCPMC7589751
OpenAlexW3096976771

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.