Researchers have made a significant discovery in understanding Parkinson’s disease: a protein called NEMO plays a vital role in preventing the condition.
This breakthrough, led by Professor Konstanze Winklhofer from Ruhr University Bochum, Germany, was published in the journal Nature Communications and opens new avenues for potential treatments.
NEMO, known for its role in the immune system, has an unexpected function in preventing Parkinson’s disease. It does this by binding to certain protein chains that signal the need for cellular waste removal, thus aiding in the breakdown of harmful protein aggregates.
Parkinson’s and other neurodegenerative diseases like Alzheimer’s are marked by the buildup of protein aggregates in the brain.
In Parkinson’s, specifically, these aggregates are primarily composed of a protein called ⍺-synuclein, leading to the formation of Lewy bodies – a hallmark of the disease. These aggregates can cause neuronal cell death and disease progression.
The research team delved into how ⍺-synuclein is degraded. Proteins meant for degradation are tagged with a chain of ubiquitin molecules. This tagging system helps the cellular waste disposal system recognize and process these proteins.
They discovered that a specific type of ubiquitin chain, known as linear ubiquitin chains, accumulates on protein aggregates in neuronal cells, reducing their toxicity.
NEMO plays a key role here by attaching to these linear ubiquitin chains on the aggregates, promoting the degradation of ⍺-synuclein.
An interesting aspect of this mechanism is its reliance on autophagy, a critical component of cellular waste removal. Autophagy involves packing materials to be degraded into vesicles that fuse with lysosomes – cell organelles equipped with degrading enzymes.
NEMO interacts with a protein in the autophagy machinery, aiding in the efficient recruitment of this machinery to protein aggregates.
A significant aspect of this study was the case of a patient with early-onset and severe Parkinson’s disease, treated by neurologists at the University of San Francisco. Genetic testing revealed a rare mutation in the patient’s NEMO gene.
This variant couldn’t bind to linear ubiquitin chains, leading to the disruption of ⍺-synuclein aggregate degradation. This case highlighted not only the importance of NEMO in protein quality control but also its broader role in neurodegenerative diseases.
This research lays the groundwork for future studies to explore how NEMO and linear ubiquitin chains could be leveraged for new therapeutic strategies against Parkinson’s and possibly other neurodegenerative diseases.
The discovery of NEMO’s role provides a new perspective on the disease and offers hope for targeted treatment approaches.
If you care about Parkinson’s disease, please read studies about Vitamin E that may help prevent Parkinson’s disease, and Vitamin D could benefit people with Parkinson’s disease.
For more information about brain health, please see recent studies about new way to treat Parkinson’s disease, and results showing COVID-19 may be linked to Parkinson’s disease.
The research findings can be found in Nature Communications.
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