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Verian Bader and Konstanze Winklhofer (right) are on the trail of the development of neurodegenerative diseases. Photo Credit: © RUB, Marquard |
Researchers have identified a mechanism that promotes the breakdown of harmful protein deposits. If it malfunctions, it can lead to Parkinson’s disease.
NEMO, a protein that is primarily associated with signaling processes in the immune system, prevents the deposition of protein aggregates that occur in Parkinson’s disease. For this purpose, it binds to certain protein chains that serve as markers for cellular waste removal, thus promoting the degradation of the harmful aggregates. A research team headed by Professor Konstanze Winklhofer from Ruhr University Bochum, Germany, has shed light on how this mechanism works. The team published their findings in the journal Nature Communications on December 19, 2023. In follow-up studies, the team is investigating ways to harness the findings for therapeutic strategies.
Looking for targeted therapeutic approaches
Neurodegenerative diseases, such as Parkinson’s or Alzheimer’s disease, are associated with the deposition of protein aggregates in the brain. These aggregates accumulate when the cellular waste removal system is defective or overloaded. In Parkinson’s disease, aggregates consisting primarily of the protein ⍺-synuclein are found in certain regions of the brain. “The fact that such aggregates occur, which are referred to as Lewy bodies, is a key feature of Parkinson’s disease,” explains Konstanze Winklhofer.
The misfolding and aggregation of ⍺-synuclein is of crucial importance for processes that lead to the loss of function and death of neuronal cells and contribute to the progression of the disease. Researchers from various disciplines around the world are therefore aiming to decipher these processes at a cellular and molecular level, in order to develop targeted therapeutic approaches.