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Copper and Iron play an important role in enhancing Alzheimer's disease

New Delhi, Wed, 21 Aug 2013 NI Wire

Separate studies have shown that Iron and copper accumulation are one of the main causes behind Alzheimer's disease.

The study conducted by researchers of Semel Institute for Neuroscience and Human Behavior at UCLA carried out the study on Iron accumulation while researchers of University of Rochester Medical Center (URMC) Department of Neurosurgery studied the effects of copper accumulation.

Dr. George Bartzokis and his colleagues studying the iron affects looked at two areas of the brain – hippocampus and thalamus.

Effects of Iron accumulation in Alzheimer’s disease:

Alzheimer damage hippocampus at an early stage while thalamus is affected in the later stages. Using sophisticated brain-imaging techniques, they found that iron is increased in the hippocampus and is associated with tissue damage in that area.

The destruction of myelin, the fatty tissue that coats nerve fibers in the brain, he says, disrupts communication between neurons and promotes the buildup of the plaques. These amyloid plaques in turn destroy more and more myelin, disrupting brain signaling and leading to cell death and the classic clinical signs of Alzheimer's.

Myelin is produced by cells called oligodendrocytes.

Although iron is essential for cell function, too much of it can promote oxidative damage, to which the brain is especially vulnerable.

The research has been published in the Journal of Alzheimer's Disease.

Effects of Copper accumulation in Alzheimer’s disease:

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.

The research team dose brain with copper over a three month period.

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.

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.

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.

(with inputs from ANI)


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