Evidence map›Paper›PMID 33291628›Full record

ReviewInternational journal of molecular sciences2020

Copper Dyshomeostasis in Neurodegenerative Diseases-Therapeutic Implications.

Grażyna Gromadzka, Beata Tarnacka, Anna Flaga, Agata Adamczyk

Open access · goldAbstract readReview
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 166 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed, 2 pooled it
14.9field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 2 syntheses or guidelines pooled it, 321 citations in OpenAlex.

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  17. Role of cuproptosis in digestive system tumors (Review).International journal of molecular medicine · 2026
    Review
  18. The pathogenesis of liver fibrosis in Wilson's disease: hepatocyte injury and regulation mediated by copper metabolism dysregulation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
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106 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Grażyna GromadzkaCollegium Medicum, Faculty of Medicine, Cardinal Stefan Wyszynski University, Wóycickiego 1/3 Street, 01-938 Warsaw, Poland.
Beata TarnackaDepartment of Rehabilitation, Eleonora Reicher National Institute of Geriatrics, Rheumatology and Rehabilitation, Rehabilitation Clinic, Medical University of Warsaw, Spartańska 1 Street, 02-637 Warsaw, Poland.ORCID 0000-0001-9902-5969
Anna FlagaCollegium Medicum, Faculty of Medicine, Cardinal Stefan Wyszynski University, Wóycickiego 1/3 Street, 01-938 Warsaw, Poland.
Agata AdamczykDepartment of Cellular Signalling, Mossakowski Medical Research Centre, Polish Academy of Sciences, 5 Pawińskiego Street, 02-106 Warsaw, Poland.ORCID 0000-0002-6867-9377
Cardinal Stefan Wyszynski University in Warsaw · PLMedical University of Warsaw · PLMossakowski Medical Research Institute, Polish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Copper is one of the most abundant basic transition metals in the human body. It takes part in oxygen metabolism, collagen synthesis, and skin pigmentation, maintaining the integrity of blood vessels, as well as in iron homeostasis, antioxidant defense, and neurotransmitter synthesis. It may also be involved in cell signaling and may participate in modulation of membrane receptor-ligand interactions, control of kinase and related phosphatase functions, as well as many cellular pathways. Its role is also important in controlling gene expression in the nucleus. In the nervous system in particular, copper is involved in myelination, and by modulating synaptic activity as well as excitotoxic cell death and signaling cascades induced by neurotrophic factors, copper is important for various neuronal functions. Current data suggest that both excess copper levels and copper deficiency can be harmful, and careful homeostatic control is important. This knowledge opens up an important new area for potential therapeutic interventions based on copper supplementation or removal in neurodegenerative diseases including Wilson's disease (WD), Menkes disease (MD), Alzheimer's disease (AD), Parkinson's disease (PD), and others. However, much remains to be discovered, in particular, how to regulate copper homeostasis to prevent neurodegeneration, when to chelate copper, and when to supplement it.

Indexed as

Disease SusceptibilityAnimalsAstrocytesBiological TransportBiomarkersBrainCopperDisease ManagementHepatolenticular DegenerationHomeostasisHumansMetabolic Networks and PathwaysNeurodegenerative DiseasesNeuronsOrgan SpecificityBiomarkersCopperAlzheimer’s diseaseastrocytescopperneurodegenerationneuronsParkinson’s diseasetreatmentWilson’s disease

Identifiers

PMID33291628
PMCPMC7730516
OpenAlexW3108197638

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.