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Metal-protein attenuation with iodochlorhydroxyquin (clioquinol) targeting Abeta amyloid deposition and toxicity in Alzheimer disease: a pilot phase 2 clinical trial.
Plain-language guide to PMID 14676042 (2003): double-blind randomized controlled trial of Zinc and Clioquinol in 2 patients.
Key Facts
- PMID
- 14676042
- Journal
- Archives of neurology
- Year
- 2003
- Study type
- Randomized Controlled Trial
- Authors
- Ritchie CW et al. (19 authors)
- DOI
- 10.1001/archneur.60.12.1685
What This Study Did, in Plain Language
What Was Tested
The paper reports a study of Zinc and Clioquinol, published as a randomized controlled trial.
To test this theory, the researchers developed a clinical intervention using clioquinol, a metal-protein-attenuating compound (MPAC) that inhibits zinc and copper ions from binding to Abeta, thereby promoting Abeta dissolution and diminishing its toxic properties.
Why It Was Studied
Alzheimer disease (AD) may be caused by the toxic accumulation of beta-amyloid (Abeta).
Who Took Part
According to the abstract, 2 patients were involved.
The age groups tagged for this paper are middle-aged adults, older adults and people over 80, both men and women.
A pilot phase 2 clinical trial in patients with moderately severe Alzheimer disease.
How the Study Was Run
The researchers set it up as a randomized, double-blind and pilot study.
Because people in this Zinc study were split into groups at random, differences between the groups are less likely to reflect who happened to join each one.
Neither the patients nor the staff measuring them knew who was on Zinc, so expectations could not easily colour the readings.
It is described as a pilot, a small early test of whether a larger Zinc study would be practical.
What Was Measured
Topics PubMed links to this paper include Alzheimer Disease, Amyloid beta-Peptides, Chelating Agents, Clioquinol, Cognition, Copper and Peptide Fragments.
What This Means in Plain Language
The paper is a randomized, double-blind and pilot study of Zinc and Clioquinol in 2 patients.
With fewer than 40 people, it is a small study, so it is better read as an early signal for further research than as a settled answer.
Its findings take up roughly 5 sentences of the abstract and are left out here on purpose; the source paper is the place to read them.
The publication is from 2003 (Archives of neurology), a journal based in United States.
More context: the related Vitamin D, K2, Magnesium and Zinc library page, all human trials.
Related Library Page
Vitamin D, K2, Magnesium and Zinc: Magnesium is described as required for AMPK to function.
Related Pages
Source: PubMed record. This explanation is written by PeptideWhiz from the public record. For research and education only. Not medical advice; no dosing information is given.