Copper may stabilize cognitive decline in patients with Alzheimer's disease, believe researchers in Germany who are conducting a clinical trial to assess the effects of supplementation.
Alzheimer's is a degenerative brain disease involving loss of cognitive function. It is characterized by a build-up of amyloid plaques in the brain, composed primarily of the A-beta peptide.
According to the Alzheimer's Association, 4.5 million Americans have Alzheimer's disease - double the number in 1980. Incidence is expected to continue rising, to reach between 11.3 and 16 million by 2050.
As the populous baby-boom generation enters its senior years, finding cheap, available means of preventing or ameliorating such conditions is important to reduce the health care burden.
Researchers at Saarland University Medical Center have commenced a phase-II clinical study involving 70 patients with mild to moderate Alzheimer's disease, who receive either 8mg of copper orotate or a placebo every day for 12 months.
The team, led by Dr Thomas Bayer, head of the neurobiology division, and Dr Frank Pajonk of the department of psychiatry, was encouraged to embark on this human study following the positive results of earlier investigations.
In a study published in the September issue of the Journal of Alzheimer's Disease (vol 8, issue 1), they measured the plasma copper levels of 32 Alzheimer's patients, and assessed their cognitive abilities using a method known as the Alzheimer's disease Assessment Scale-cognitive subscale.
All of the patients were found to have plasma copper levels of between 65 and 165 µg/dL. In 87.5 percent of the patients, there was a significant correlation between plasma copper and cognitive ability. Those with medium plasma copper levels made fewer mistakes in the memory test than those with low plasma copper levels.
"This finding supports the hypothesis of a mild copper deficiency in most Alzheimer's disease patients," wrote the researchers.
As part of this study, they also measured the amount of copper in tap water taken from the homes of all the participants. Interestingly, there was no correlation between copper levels in the water and the patient's plasma copper levels.
Dr Bayer and his team have also carried out a clinical trial on dietary copper intake in a mouse model, which was published in the Proceeds of the National Academy of Science in 2003 (Nov 25;100(24):14187-92). In this instance, copper in the drinking water of Alzheimer's mice was found to slow the progression of the disease.
Dr Bayer noted that their survival rate increased, their A-beta levels decreased, their brain copper levels increased (indicating that the copper was, indeed, reaching the brain), and copper was also finding its way to cells that have enzymes needing copper in order to function.
As for the current phase-II trial, Dr Bayer told NutraIngredients-USA.com that 15 patients have so far competed the course, but no preliminary results are available as the double-blind control is still in place. The remaining patients will all have completed this phase by the end of 2006. As well as the copper orotate or the placebo, all are also receiving a standard cholinesterase inhibitor.
After the initial 12 months, the patients have the opportunity to continue with a further 12-month open label study, in which they take the copper supplements. So far, all 15 patients have chosen to continue with second phase.
Dr Bayer was clear to point out that copper supplementation is thought only to be relevant in cases where Alzheimer's has already been diagnosed. Taking copper as a precautionary measure in advance of diagnosis is not believed to be useful - and may even prove detrimental to health since it can be liver toxic.
The patients taking part in the study are monitored for liver toxicity. So far, there have been no-drop outs on the grounds of adverse reaction and the dose of copper administered is believed to be safe.