WASHINGTON, Aug. 19 (Xinhua) -- Copper appears to be one of the main environmental factors linked to Alzheimer's disease, the most common form of dementia among older people, according to a study released Monday in the journal Proceedings of the National Academy of Sciences.
Researchers from the University of Rochester found that copper can trigger the onset and enhance the progression of Alzheimer's disease by preventing the clearance and accelerating the accumulation of toxic proteins in the brain.
"It is clear that, over time, copper's cumulative effect is to impair the systems by which amyloid beta is removed from the brain, " said Rashid Deane, a research professor with the University of Rochester and lead author of the study.
"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," he said.
Copper is found in drinking water carried by copper pipes, nutritional supplements, and in certain foods such as red meats, shellfish, nuts, and many fruits and vegetables. The mineral plays an important and beneficial role in nerve conduction, bone growth, the formation of connective tissue, and hormone secretion.
The researchers found that copper can also accumulate in the brain and cause the blood brain barrier, the system that controls what enters and exits the brain, to break down, resulting in the toxic accumulation of the protein amyloid beta, a by-product of cellular activity.
Using both mice and human brain cells, Deane and his colleagues conducted a series of experiments that have pinpointed the molecular mechanisms by which copper accelerates the pathology of Alzheimer's disease.
Under normal circumstances, amyloid beta is removed from the brain by a protein called lipoprotein receptor-related protein 1 ( LRP1). But the researchers observed that copper disrupted the function of LRP1 through a process called oxidation which, in turn, inhibited the removal of amyloid beta from the brain.
The researchers then looked at the impact of copper exposure on mouse models of Alzheimer's disease. In these mice, the cells that form the blood brain barrier have broken down and become "leaky," a likely combination of aging and the cumulative effect of toxic assaults, allowing elements such as copper to pass unimpeded into the brain tissue.
They observed that copper stimulated activity in neurons that increased the production of amyloid beta. The copper also interacted with amyloid beta in a manner that caused the proteins to bind together in larger complexes creating logjams of the protein that the brain's waste disposal system cannot clear.
In addition, the researchers observed that copper provoked inflammation of brain tissue which may further promote the breakdown of the blood brain barrier and the accumulation of Alzheimer's-related toxins.
However, because metal is essential to so many other functions in the body, the researchers said that these results must be interpreted with caution.
"Copper is an essential metal and it is clear that these effects are due to exposure over a long period of time," said Deane. "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."