The Free Press, Mankato, MN

State, national news

August 20, 2013

Copper may play key role in Alzheimer's disease


Deane said that, in the absence of effective treatments for Alzheimer’s disease, his team’s findings suggest a way to prevent the memory-robbing disorder or slow it once it has taken hold. One drug candidate currently in Phase 2 trials — an agent that binds with copper molecules and escorts them out of the body — might well do that, said the study’s lead author. But even now, Deane said, consumers could be checking their vitamin supplements for copper and researching whether their water filters are equipped to remove copper from their drinking supply.

“The key will be striking the right balance between too much and too little copper consumption,” Deane said. “Right now, we cannot say what the right level will be. But diet may one day play an important role in regulating this process.”

Deane’s team worked with mice and with human brain cells that play a key role in forming the blood-brain barrier to detect the mechanisms by which copper might start, drive or worsen Alzheimer’s disease. They noted that in the elderly, the blood-brain barrier becomes “leaky,” letting in larger toxic molecules circulating the blood. So too does the concentration of copper in the brain’s small blood vessels increase with age.

Starting in the mouse-equivalent of young adulthood, they fed mice a regular diet, but gave half of them water that contained levels of copper equal to one-tenth the maximum allowed by the Environmental Protection Agency. The other half were given double-distilled water with a very low copper content — less than 2 percent of that given to the high-copper group. In a second experiment, older mice bred for their propensity to develop beta-amyloid plaques were fed the copper-tainted water or the low-copper water.

After three months, the effects were dramatic: In the mice who took in high doses of copper, the scientists observed that copper accumulated in the small blood vessels of the brain. Compared to mice on low doses of copper, the high-copper mice showed four times fewer levels of a protein called LRP1, which transports beta-amyloid and other debris out of the brain. They also showed abnormally high levels of beta-amyloid production and of neuro-inflammation.

As they aged, the brains of mice who were fed high doses of copper had beta-amyloid levels on par with those of mice who drank low-copper water but had been bred to develop beta-amyloid at high rates.


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