Evidence map›Paper›PMID 11994023›Full record

ReviewCNS drugs2002

The role of iron and copper in the aetiology of neurodegenerative disorders: therapeutic implications.

George Perry, Lawrence M Sayre, Craig S Atwood, Rudolph J Castellani, Adam D Cash, Catherine A Rottkamp, Mark A Smith

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
8.6field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 133 citations in OpenAlex.

  1. Pooled it
  2. Amyloid-International journal of molecular sciences · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. A Peroxynitrite Dicopper Complex: Formation via Cu-NO and Cu-OJournal of the American Chemical Society · 2016
    Article
  8. Article
  9. Article
  10. Article
  11. Mechanisms of neurodegeneration shared between multiple sclerosis and Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2011
    Review
  12. Role of metal dyshomeostasis in Alzheimer's disease.Metallomics : integrated biometal science · 2011
    Review
  13. Iron and mechanisms of neurotoxicity.International journal of Alzheimer's disease · 2010
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Expression of a mutant form of the ferritin light chain gene induces neurodegeneration and iron overload in transgenic mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008
    Article
  19. Article
  20. Article
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 at 1 institution in 1 country.

George PerryInstitute of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, USA. gxp@po.cwru.edu
Lawrence M Sayre
Craig S Atwood
Rudolph J Castellani
Adam D Cash
Catherine A Rottkamp
Mark A Smith
Case Western Reserve University · US

Funding

CYTOSKELETAL OXIDATIVE MODIFICATIONSR01AG014249 · NIA · CASE WESTERN RESERVE UNIVERSITY · PI ANDERSON, VERNON E. · 1997 to 2004
$1.3M
METABOLIC ABNORMALITIES IN ALZHEIMER DISEASER01NS038648 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SMITH, MARK A · 1999 to 2002
$571k
NIA NIH HHS AG14249NINDS NIH HHS NS38648
6 · The paper itself

Abstract

Abnormalities in the metabolism of the transition metals iron and copper have been demonstrated to play a crucial role in the pathogenesis of various neurodegenerative diseases. Metal homeostasis as it pertains to alterations in brain function in neurodegenerative diseases is reviewed in this article in depth. While there is documented evidence for alterations in the homeostasis, redox-activity and localisation of transition metals, it is also important to realise that alterations in specific copper- and iron-containing metalloenzymes appear to play a crucial role in the neurodegenerative process. These changes provide the opportunity to identify pathways where modification of the disease process can occur, potentially offering opportunities for clinical intervention. As understanding of disease aetiology evolves, so do the tools with which diseases are treated. In this article, we examine not only the possible mechanism of disease but also how pharmaceuticals may intervene, from direct and indirect antioxidant therapy to strategies involving gene therapy.

Indexed as

Alzheimer DiseaseAmyotrophic Lateral SclerosisAntioxidantsChelating AgentsCopperFree RadicalsHomeostasisHumansIronNeurodegenerative DiseasesOxidation-ReductionOxidative StressParkinson DiseasePrion DiseasesAntioxidantsChelating AgentsCopperFree RadicalsIron

Identifiers

PMID11994023
OpenAlexW2227557146

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.