Home › Research › Treatments
[The role of copper in the pathophysiology of Alzheimer's disease]
Kessler H, Pajonk FG, Supprian T, Falkai P, Multhaup G, Bayer TA.. Der Nervenarzt, 2005-05-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's dementia (AD) is a chronically progressive neurodegenerative disease. The key protein in the pathophysiology of AD is the amyloid precursor protein (APP) which releases the amyloid-beta peptide (Abeta) by proteolytic cleavage. APP is probably involved in the homeostasis of cellular copper (Cu) metabolism, because significantly changed Cu levels in the brain were found in AD patients as well as in mouse models. In vivo studies with transgenic mice showed that oral Cu supplements can restore lowered Cu levels in the brain to normal, can reduce Abeta production, and can reduce mortality of the animals. Currently, the influence of oral Cu supplementation (in addition to an established acetylcholinesterase inhibitor) on the progression of the disease is being studied in a prospective, double-blind, randomized and placebo-controlled longitudinal clinical trial in patients with mild AD.
Key findings
- APP is probably involved in the homeostasis of cellular copper (Cu) metabolism, because significantly changed Cu levels in the brain were found in AD patients as well as in mouse models.
- In vivo studies with transgenic mice showed that oral Cu supplements can restore lowered Cu levels in the brain to normal, can reduce Abeta production, and can reduce mortality of the animals.
Why it matters
This paper describes how copper metabolism may relate to Alzheimer's disease, noting that copper levels are changed in patients and mouse models. In mice, oral copper supplements restored brain copper, reduced amyloid-beta production, and reduced mortality, and a human trial in mild Alzheimer's was underway at the time.
New to this subject? Start with our plain-English guide: Treatments →
Study details
- Study designlongitudinal study
- Evidence strengthHigh
How this study scored 41/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Der Nervenarzt) |
| Journal's citation record | 0 / 4 | Der Nervenarzt: journal h-index 61 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2005 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 2 / 7 | Cited 14 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.6 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 1 / 6 | Cited 0.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 1 other studies in this library |
| Still being cited | 0 / 4 | Cited 0 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Thomas A. Bayer: h-index 75 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Freie Universität Berlin: institution h-index 744 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15905983) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
May need a subscription Unpaywall, Europe PMC and OpenAlex found no free copy of the full text (checked 10 Oct 2026), so the publisher may charge for it. The PubMed abstract is free.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Kessler, H., Pajonk, F. G., Supprian, T., Falkai, P., Multhaup, G., & Bayer, T. A. (2005). [The role of copper in the pathophysiology of Alzheimer's disease]. Der Nervenarzt. https://doi.org/10.1007/s00115-004-1849-6
Vancouver
Kessler H, Pajonk FG, Supprian T, Falkai P, Multhaup G, Bayer TA. [The role of copper in the pathophysiology of Alzheimer's disease]. Der Nervenarzt. 2005. doi:10.1007/s00115-004-1849-6. PMID: 15905983.
BibTeX
@article{kessler2005-15905983,
author = {Kessler, H. and Pajonk, F. G. and Supprian, T. and Falkai, P. and Multhaup, G. and Bayer, T. A.},
title = {{[The role of copper in the pathophysiology of Alzheimer's disease]}},
journal = {Der Nervenarzt},
year = {2005},
doi = {10.1007/s00115-004-1849-6},
pmid = {15905983},
url = {https://doi.org/10.1007/s00115-004-1849-6}
}
Studies this one cites
Referenced by this study and also in the alzhub library, so you can read them here.
Later studies that cite this one
1 study in the alzhub library lists this one in its references.
Related studies in Treatments
Also in Treatments
166 studies in the library are filed under Treatments with no topic tag they share with another; these are this study's neighbours in a fixed tour of them. The Treatments hub.