Is copper the bad boy in Alzheimer’s disease?

Man has been using copper for thousands of years including fashioning it for jewellery items and for conduits to carry water as pipes, jugs and cookware.

It is also an essential trace mineral found in all human tissue. My Mum swears by her copper bracelet in helping her to overcome some of the pain associated with her arthritis. 

There is something rather pleasing about the warm slightly pinky colour of copper that turns green with age.

We need copper too. In the human body it works with iron to form red blood cells and is essential for healthy blood vessels, bones and our immune system.

It is found naturally occurring in many foods including red meat – kidneys and liver, shellfish such as oysters, whole-grains nuts, dark leafy vegetables, prunes, cocoa, black pepper and yeast and some fruit and vegetables.

Too much copper can be toxic. One condition called Wilson’s disease (very rare) is an inherited disorder where excess copper is deposited in the liver, brain and other organs and can cause liver, brain and other problems.

Too little copper is linked to anaemia and osteoporosis.

A new study has recently been published in the journal Proceedings of the National Academy of Sciences which indicates that copper may be a significant environmental factor involved in triggering the onset and enhancing the progression of Alzheimer’s disease by preventing and accelerating the accumulation of toxic proteins in the brain.

If this is the case then further study will need to be undertaken to determine how much copper is too much and what can be done to detect excess levels and manage it appropriately.

This study’s findings at first glance appear to contradict findings published by researchers at Keele University in the UK earlier this year where they reported that copper at levels commonly found in the brain probably protects against the formation of amyloid plaques.  Their suggestion was that it might be lower levels of copper in the brain that promote the damage.

In an age where the number of people being diagnosed with Alzheimer’s disease is increasing rapidly, there is a great deal of interest in trying to find out more about what causes the condition and what can be done to help treat it more effectively.

Hence I think it is really important not to jump to any conclusions prematurely as a result of this study. The media have already latched onto it and proclaiming headlines suggestive that copper is the culprit here, let’s all get rid of the copper, which of course is nonsense.

When a purported link between aluminium and Alzheimer’s disease was made a number of years ago, thousands of people threw out their aluminium saucepans and stopped using aluminium based antiperspirant deodorants. It took many years and many more studies to undo that link which was ultimately deemed to be wrong.

One study does not prove anything. The results need to be examined and replicated and investigated further before any conclusion can be more rigorously drawn.

Meanwhile let us look at what this study found:

The study was performed on mice and revealed how copper can accumulate in the brain, causing the blood brain barrier – the sophisticated barrier that restricts what can or cannot pass across into the brain, to break down. This then allows a toxic build up of beta amyloid to accumulate. Beta amyloid is a normal by product of cellular activity but in Alzheimer’s disease excessive amounts of this are found as amyloid plaques.

The body normally gets rid of excess beta amyloid using a protein called LRP1 (lipoprotein receptor-related protein) that occurs in the capillaries supplying the brain, by binding to the amyloid and escorting it (a bit like the bouncer in a night club) out of the brain and into the blood stream.

Dosing the mice with copper at levels that would be similar to one tenth of what we as humans would normally consume in our water according to current water quality standards, resulted in the copper interfering with LRP1 function by an oxidative process. The paper also reported showing the same effect in human brain cells. In other words the normal amyloid clearance system was impaired.

Moreover in those mice with Alzheimer’s disease the blood brain barrier was seen to be impaired by a combination of ageing and accumulation of what they called toxic assaults allowing excess copper to pass into the brain. Here the copper was observed to stimulate the production of beta amyloid and in addition adding insult to injury caused the excess amyloid to bind together in clumps making it harder for the brain to clear.

What remains unclear to me is why it is the lower amounts of copper that appear to cause the damage, not higher.

This study’s findings do appear important, they do however require clarification as to what this means to us, and the implications that will need to be addressed in the future.

Refs:

Trumbo P, Yates AA, Schlicker S, Poos M. Food and Nutrition Board, Institute of Medicine, The National Academies. Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc. J Am Diet Assoc. 2001 Mar;101(3):294-301.

Mason JB. Vitamins, trace minerals, and other micronutrients. In: Goldman L, Ausiello D, eds. Cecil Medicine. 24th ed. Philadelphia, Pa: Saunders Elsevier; 2011:chap 225.

Matthew Mold, Larissa Ouro-Gnao, Beata M Wieckowski, Christopher Exley. Copper prevents amyloid-β1–42 from forming amyloid fibrils under near-physiological conditions in vitro. Scientific Reports, 2013; 3 DOI: 10.1038/srep01256

Itender Singh, Abhay P. Sagare, Mireia Coma, David Perlmutter, Robert Gelein, Robert D. Bell, Richard J. Deane, Elaine Zhong, Margaret Parisi, Joseph Ciszewski, R. Tristan Kasper, and Rashid Deane. Low levels of copper disrupt brain amyloid-β homeostasis by altering its production and clearance. PNAS, August 19, 2013 DOI: 10.1073/pnas.1302212110

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