2023-12-26 04:19:00
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At least 200,000 people in Germany suffer from Parkinson’s. Scientists have now made a breakthrough in decoding the processes behind it.
Parkinson’s, like dementia, is one of the so-called neurodegenerative diseases. These are characterized by the deposition of protein aggregates (mainly consisting of protein α-synuclein) in certain brain regions. In the event of a defect or overload of the cellular waste disposal system, which according to information from Max-Planck-Gesellschaft However, as the waste is constantly disposed of inside the cells of the human body, the aggregates accumulate. This in turn leads to loss of function and death of the nerve cells and ultimately to the progression of Parkinson’s disease.
Researchers from the Ruhr University Bochum (RUB) have now succeeded in finding out new insights into the mechanism behind the breakdown of α-synuclein German medical journal reported. These could help to develop targeted therapeutic approaches to treat Parkinson’s in the future.
Parkinson’s: Researchers discover mechanism behind neurodegenerative disease
New findings from Parkinson’s research can help in the development of targeted therapy. © Zoonar.com/Kasper Ravlo/IMAGO
In your Studywhich is in the specialist magazine nature communications was published, a research team led by Prof. Dr. Konstanze Winklhofer discovered that cellular proteins that are intended for degradation are tagged with a chain of small ubiquitin molecules. This allows the proteins to be identified by garbage disposal. “Depending on the type of connection between these ubiquitin molecules and the length and structure of the ubiquitin chains, the cellular waste disposal system can recognize which processes should be used to degrade the marked proteins,” says Winklhofer, according to one Press release the RUB. So-called linear ubiquitin chains are enriched on protein aggregates in nerve cells. They reduce the toxicity of protein aggregates.
The mechanism behind this protective effect has been recognized by scientists. It turned out that the NEMO protein docks to linear ubiquitin chains on the protein aggregates and promotes the degradation of α-synuclein. However, the protective effect of NEMO is blocked by inhibiting what is known as autophagy. This is an important component of cellular waste disposal. The research team ultimately found that NEMO interacts with a protein in the autophagy machinery.
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Parkinson’s disease: Severe illness caused by a mutation in the NEMO gene
According to Winklhofer, the groundbreaking case for the study was a case of a patient who was cared for by neurologists in the USA. The person affected suffers from one progressive Parkinson’s disease, which she became ill with when she was in her early 40s. A genetic test revealed that the patient had a rare mutation in the NEMO gene. This NEMO variant could not bind to linear ubiquitin chains and therefore could not dock to protein aggregates. This led to a pronounced deposition of α-synuclein aggregates in the patient’s brain.
In addition, other protein aggregates were also detectable, such as those that occur in Alzheimer’s disease, said Winklhofer and continued: “This explains the serious course of the NEMO-associated disease and supports a general role of NEMO in the quality control of aggregated proteins.”
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This article only contains general information on the respective health topic and is therefore not intended for self-diagnosis, treatment or medication. It in no way replaces a visit to the doctor. Unfortunately, our editorial team cannot answer individual questions about medical conditions.
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