Parkinson’s Breakthrough: A Recent Discovery Could Lead to New Treatments



Parkinson's disease does not yet have any disease-modifying medicines that can change how the disease develops. A team of professionals from all around the world are working to change that under the direction of researchers at the University of Colorado Anschutz Medical Campus.

They just released a new study in the journal Brain that advances understanding of the key protein known as -synuclein (Syn), which they discovered links Parkinson's disease and inflammation.                                                                    
Neurodegenerative illnesses like Parkinson's disease and Lewy body dementia have been connected to the protein Syn, which is mostly produced in neurons. In this new study, a novel mechanism involving interferon activation and neuronal Syn function is identified as a potential initiator of Parkinson's disease.                          
"It's imperative to comprehend more about the factors that contribute to the onset of Parkinson's disease and how inflammation may interact with disease-related proteins. According to David Beckham, MD, associate professor in the department of infectious disease at the University of Colorado School of Medicine, which is located on the CU Anschutz Medical Campus, "With this information, we could potentially provide new approaches for treatments by altering or interfering with these inflammatory pathways that may act as a trigger for the disease."

The researchers infected human and mouse dopaminergic neurons with an RNA virus in order to study the mechanism of Syn-induced immune responses to viral infections in the brain. They found that Syn is necessary for interferon-stimulated gene expression in neurons (ISGs). Then, they discovered that Syn interacts with signaling proteins in neurons to induce the expression of ISGs in response to any stimuli that results in interferon signals, a subtype of immunological response.

The protein Syn, which has been linked to the onset of Parkinson's disease, and inflammation are now clearly linked for the first time by this study.

The researchers claim that these results show that Syn reacts to inflammatory and infectious pathways and that this relationship may play a significant role in the onset of Parkinson's disease. The most important next step is to determine whether interactions between interferon and Syn lead to the toxic fibrils of misfolded Syn that have been discovered in Parkinson's disease.

Future research, according to the researchers, is required to examine the relationships between type 1 interferon signals in neurons and misfolded Syn to ascertain whether medications that block these connections can stop the development of misfolded Syn. As a result, patients would require a therapy strategy that might potentially modify their illness.

Alpha-synuclein supports type 1 interferon signaling in neurons and brain tissue, according to a study published on July 21st, 2022, in the journal Brain by Brendan Monogue, Yixi Chen, Hadrian Sparks, Ranya Behbehani, Andrew Chai, Alexander J Rajic, Aaron Massey, B K Kleinschmidt-Demasters, Matthieu Vermeren, Tilo Kunath, and J David Beckham.

By UNIVERSITY OF COLORADO ANSCHUTZ MEDICAL CAMPUS  

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