Evidence map›Paper›PMID 18972062›Full record

Trial reportJournal of neural transmission (Vienna, Austria : 1996)2008

Effect of copper intake on CSF parameters in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial.

Holger Kessler, Frank-Gerald Pajonk, Daniela Bach, Thomas Schneider-Axmann, Peter Falkai, Wolfgang Herrmann, Gerd Multhaup, Jens Wiltfang, Stephanie Schäfer, Oliver Wirths and 1 more

Open access · hybridAbstract readClinical Trial, Phase IIRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Journal of neural transmission (Vienna, Austria : 1996), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

21 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Metals in Alzheimer's Disease.Biomedicines · 2023
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Disturbed copper bioavailability in Alzheimer's disease.International journal of Alzheimer's disease · 2011
    Article
  18. Copper modulation as a therapy for Alzheimer's disease?International journal of Alzheimer's disease · 2011
    Article
  19. Article
  20. Copper in the brain and Alzheimer's disease.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2010
    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

11 authors at 4 institutions in 1 country.

Holger KesslerDepartment of Psychiatry and Psychotherapy, Saarland University Hospital, Homburg/Saar, Germany.
Frank-Gerald Pajonk
Daniela Bach
Thomas Schneider-Axmann
Peter Falkai
Wolfgang Herrmann
Gerd Multhaup
Jens Wiltfang
Stephanie Schäfer
Oliver Wirths
Thomas A Bayer
University of Göttingen · DESaarland University · DEFreie Universität Berlin · DEUniversity of Duisburg-Essen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer's disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on CSF biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Abeta42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Abeta42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Abeta42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Abeta42 levels declined significantly in both groups within 12 months supporting the notion that CSF Abeta42 may be valid not only for diagnostic but also for prognostic purposes in AD.

Indexed as

AgedAlzheimer DiseaseAmyloid beta-PeptidesBiomarkersBrainCognitionCognition DisordersCopperDouble-Blind MethodDown-RegulationFemaleHumansMaleNeuropsychological TestsOutcome Assessment, Health CarePeptide FragmentsAmyloid beta-Peptidesamyloid beta-protein (1-42)BiomarkersCopperPeptide FragmentsPlacebostau Proteins

Identifiers

PMID18972062
OpenAlexW2016822949

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.