Copper is an integral component of cuproproteins required for many physiological functions. The mineral plays an important and beneficial role in nerve conduction, bone growth, the formation of connective tissue and hormone secretion.
However, the recent study published in the journal Proceedings of the National Academy of Sciences (PNAS), suggests that copper appears to 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 in the University of Rochester Medical Center (URMC) Department of Neurosurgery, member of the Center for Translational Neuromedicine, and the lead author of the study.
The researchers observed that the copper disrupted the function of lipoprotein receptor-related protein 1 (LRP1)* through a process called oxidation which, in turn, inhibited the removal of amyloid beta from the brain. They observed this phenomenon in both mouse and human brain cells.
* LRP1 is a protein that under normal circumstances removes amyloid beta from the brain. These proteins– which line the capillaries that supply the brain with blood– bind with the amyloid beta found in the brain tissue and escort them into the blood vessels where they are removed from the brain.
They also observed that the 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.
This one-two punch, inhibiting the clearance and stimulating the production of amyloid beta, provides strong evidence that copper is a key player in Alzheimer’s disease. 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.
The researchers say that these results must be interpreted with caution, because “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.”
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