Faulty regulation of copper levels in tissues plays a major role in a wide range of illnesses, including Alzheimer’s disease, Parkinson’s disease, and motor neuron disease. An investigation of molecules that carry copper in the bloodstream has provided new leads for diagnosis and treatment.
The metal copper is crucial for a healthy metabolism, and yet, scientists know surprisingly little about how the body transports it and maintains optimum levels in tissues.
Bonded to protein molecules, copper is a vital component of numerous enzymes that catalyze key metabolic reactions.
“Biochemists have known about the importance of copper in the human body for a long time, but even they do not know, for example, how this element reaches from our food to the right destinations, i.e., various copper enzymes,” says Prof. Peep Palumaa, head of the Research Group of Metalloproteomics at Tallinn University of Technology in Estonia.
Copper is present in trace amounts throughout the body. The highest concentrations occur in areas of the body that have extremely high activity, such as the liver, brain, heart, kidneys, and skeletal muscle.
Among its many roles, the metal is vital for producing energy during cell respiration, making red blood cells, mounting immune responses, and maintaining nerve cells.
In excess, however, it can trigger the production of destructive free radicals and contribute to inflammation.
Research has linked the faulty regulation of copper levels to several neurodegenerative illnesses, including Menkes syndrome, motor neuron disease, Parkinson’s disease, and Alzheimer’s disease.
A study that Medical News Today reported on in 2013, for example, found that when copper accumulates in the brain, it promotes the development of the beta-amyloid plaques that are the hallmark of Alzheimer’s disease.
The study found that copper not only inhibits the removal of soluble beta-amyloid molecules from the brain but also encourages them to clump together to form insoluble plaques.
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