Does Copper Cause Alzheimer's? Study Shows The Metal Triggers And Encourages Development Of Toxic Amyloid Beta Proteins
Copper, among other metals, is essential to the human body. It helps the body metabolize iron, in addition to aiding nerve conduction. Deficiencies in the element can lead to immunity and bone problems such as anemia and osteoporosis. But while too much copper can also lead to problems, including kidney and intestine disease, even the trace amounts that humans consume each day may be enough to trigger and encourage the development of Alzheimer’s disease in the brain, according to a new study.
Alzheimer’s disease is the most common form of dementia. It normally begins to appear in people older than 65 years old and develops progressively as sticky amyloid-beta protein molecules clump up into larger plaques within the brain. These plaques block cell-to-cell signaling and have also been implicated in cell damage and death.
Researchers found that, over time, copper can disrupt the brain’s ability to remove these amyloid beta molecules. A normally functioning brain is able to remove amyloid beta with another protein molecule called lipoprotein receptor-related protein 1 (LRP1). The proteins typically line the capillaries, which are essential in supplying the brain with blood, and bind with amyloid beta in the brain. Once they’ve become a unit, they enter the bloodstream and move out of the brain.
Copper's One-Two Punch On The Brain
Experiments on both human and mice brain cells showed that copper disrupted these mechanisms. Researchers gave mice water with traces of copper — copper can get into water through pipes or other sources — that were one-tenth the level of the Environmental Protection Agency’s (EPA) standards, which are 1.3 milligrams/liter, over the course of three months. The copper entered their bloodstream and accumulated in the cellular walls of their brain’s capillaries.
The accumulating copper ended up impeding the production of LRP1 in mice and human capillary cells through oxidation processes, leading to a disruption in the amyloid beta removal processes. But the copper proved to be even more damaging, as it not only disrupted LRP1 production, but also stimulated neurons that increased production of amyloid beta. Then, the copper interacted with the new amyloid beta molecules and helped with binding them together.
"It is clear that, over time, copper's cumulative effect is to impair the systems by which amyloid beta is removed from the brain," Dr. Rashid Deane, a research professor at the University of Rochester Medical Center, said in a statement. "This impairment is one of the key factors that cause the protein to accumulate in the brain and form the plaques that are the hallmark of Alzheimer's disease."
Metals In The Body And In Our Food
Copper and other metals, such as iron, can be a “double-edged sword,” James O’Connor, professor and vice chairman of neurosurgery at Penn State University, told The Wall Street Journal regarding another study, which found that mice bred without a brain protein known as “tau” accumulated iron in their brains. As the iron levels increased, the mice showed more signs of Alzheimer’s symptoms. But at the same time, he says, iron interacts with oxygen to help the body generate energy.
Deane and his team of researchers, however, warn about quitting all consumption of foods with copper, since the element is integral to our body’s other functions. In fact, copper is found in many common foods, including oysters, sesame seeds, chocolate, calamari, sun dried tomatoes, nuts, and meats.
“Copper is an essential metal and it is clear that these effects are due to exposure over a long period of time,” Deane said in the statement. “The key will be striking the right balance between too little and too much copper consumption. Right now we cannot say what the right level will be, but diet may ultimately play an important role in regulating this process.”
Source: Deane R, Singh I, Sagare A, et al. Low levels of copper disrupt brain amyloid-β homeostasis by altering its production and clearance. PNAS. 2013.