Some environmental science reports are easy to interpret but others require much more care. However, it remains GallonDaily’s view that information on emerging issues should be made public and that the public should be helped to understand that just because something is being reported does not mean that it is a fact but it also does not mean that it is necessarily a fallacy.
We are drawn to mention this by a newly published research report in the prestigious Proceedings of the National Academy of Sciences that indicates that there may be a link between ingestion of copper and development of Alzheimer’s disease, a significant cause of serious dementia in elderly people.
It is early days for this research. The laboratory research was carried out on mice, not humans, and it could be that humans respond differently when exposed to copper. We need very small amounts of copper for our bodily functioning and the effect may only show up at higher levels than we are normally exposed to. The conventional dose-response linkage, the higher the dose the greater the adverse effect, probably does not apply, though recently this supposed linkage has been shown not to apply in a number of other cases. It may be that not all humans respond the same way to copper and, even if we do all respond the same way, it may be that different concentrations produce different results in different people. There may be different types of Alzheimer’s disease and copper may only influence one or several of them. As Alzheimer’s is a disease affecting the brain diagnosis is difficult or impossible until the patient has died.
In other words there is much more that we do not know than we know. However, if we were involved in an industry that uses copper in ways that expose people to it, most likely through drinking water, I would be thinking that this research may be the beginning of something important and that in some number of years I may have to make changes to my product or to its marketing.
The research comes from the University of Rochester Medical Center in Rochester, New York. Researchers there have found that a protein known amyloid-β (Aβ) accumulates in the brain of normal animals dosed with low levels of copper. The study was looking for the mechanism for this accumulation and found that copper regulates low-density lipoprotein receptor-related protein mediated Aβ clearance across the blood–brain barrier (BBB) in normal mice. Faulty Aβ clearance across the BBB due to increased Cu levels in the aging brain vessels may lead to accumulation of neurotoxic Aβ in brain tissue.
The research team speculates that copper-specific chelating agents, chaperones, or antioxidants may reduce copper-induced Aβ accumulation in brain, which should, by extension, prevent Aβ accumulation in brain tissue and improve cognition in Alzheimer’s disease.
An abstract and the research report may be accessed at http://www.pnas.org/content/early/2013/08/14/1302212110.abstract?sid=a85cbc1a-2cfe-4c11-a38e-970d1d0e103e