The study by University of Rochester Medical Center (URMC) Department of Neurosurgery showed that copper can accumulate in the brain and cause the blood brain barrier 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 researchers conducted a series of experiments that have pinpointed the molecular mechanisms by which copper accelerates the pathology of Alzheimer's disease.
The research team - "dosed" normal mice with copper over a three month period. The exposure consisted of trace amounts of the metal in drinking water and was one-tenth of the water quality standards for copper established by the Environmental Protection Agency.
The researchers found that the copper made its way into the blood system and accumulated in the vessels that feed blood to the brain, specifically in the cellular "walls" of the capillaries.
They observed that the copper disrupted the function of 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.
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 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 study is published in the journal Proceedings of the National Academy of Sciences.
--ANI (Posted on 20-08-2013)