Does copper increase the risk of Parkinson’s? – Wissenschaft.de

In Parkinson’s disease, the dopamine-producing nerve cells in the brain die. This leads to a lack of dopamine, which causes the typical muscle tremors. Despite intense research, the causes of the disease are still not entirely clear. Researchers have now shown that copper ions help a certain protein in the brain, called alpha-synuclein, to clump together. Clumps of this protein have previously been linked to nerve cell death in Parkinson’s disease. The new findings could help develop early detection tests. They are also a further step towards a causal treatment of the disease.

Parkinson’s is the second most common neurodegenerative disease in the world after Alzheimer’s. Previous therapeutic approaches aim to compensate for the lack of dopamine in the brain with drugs. In the early stages, symptoms can be relieved. However, drugs cannot stop the progressive breakdown of nerve cells. A causal treatment is not yet possible because the causes of Parkinson’s have not yet been clarified in detail. Researchers have long suspected that environmental influences such as pesticides contribute to the disease. The vital trace element copper is also discussed as an influencer.

I suspect copper

A team led by Olena Synhaivska of the Swiss Federal Laboratories for Materials Research and Testing (Empa) in Dübendorf, Switzerland, has now taken a closer look at the role of copper in the development of Parkinson’s disease. Copper is ingested through food and plays important functions in cellular metabolism. Among other things, it plays an important role in bone growth, in the transmission of stimuli in nerve cells and in the production of hormones. In the brain, however, it has an ambiguous effect: in relation to Alzheimer’s disease, it has already been discussed as both a risk factor and a protective factor, and may even be involved in the development of Parkinson’s disease.

Synhaivska and his colleagues focused on the interactions of copper ions with the alpha-synuclein protein. This protein is normally water soluble, but is sometimes present in an abnormal, clumped form in people with Parkinson’s disease. To find out how copper affects alpha-synuclein aggregation, the researchers first artificially produced the protein and observed it in the test tube. With the help of atomic force microscopy, they visualized how the protein initially formed single insoluble strands over the course of the ten-day observation period, which eventually clustered together to form a dense network.

Accelerated aggregation

In another experimental approach, the researchers added copper ions to the alpha-synuclein solution and observed its effects. “High doses of copper appear to accelerate the aggregation process,” reports Peter Nirmalraj, a colleague of Synhaivska. In addition to the faster-forming protein strands, the researchers discovered another abnormal form of alpha-synuclein in the copper-mixed solution: after a few hours, ring-shaped structures of about seven nanometers were formed. These so-called oligomers have previously been associated with nerve cell damage.

Since oligomeric rings form at the very beginning of the conversion of healthy alpha-synuclein into diseased lumps, Nirmalraj hopes they can be used as targets for new therapeutic approaches. Furthermore, the findings could help develop a diagnostic test with which Parkinson’s can be detected in the early stages, for example if the ring-shaped variant of alpha-synuclein could be detected in CSF samples.

Source: Olena Synhaivska (Federal Institute for Materials Research and Testing, Switzerland) et al., ACS Chemical Neuroscience, doi: 10.1021 / acschemneuro.2c00021

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