Parkinson’s disease occurs when certain antiviral receptors in the brain called the interferon beta pathway and their proteins are not functioning properly. As a result, the pathway is blocked, and as a result, brain cells gradually begin to die.
With scientists Private company A new study at the University of Copenhagen is developing a drug that targets another protein, but that effort may prove inadequate for most patients.
“According to our research, targeting front runners with Parkinson’s disease Drug development, NS α-synuclein protein, May not be sufficient to treat the patient or relieve symptoms. Instead, key considerations need to be made to resolve the brain inflammation caused by dysfunctional interferon beta receptor signaling, “said Shohreh Issazadeh, Principal Investigator and Corresponding Author of the Study. -Professor Navikas explains.
The α-synuclein protein has long been considered to be a toxic protein for removal in Parkinson’s disease. However, studies conducted in mice suggest that it may only be useful in well-known forms of Parkinson’s disease, including a few percent of all cases of Parkinson’s disease, but so-called sporadic. The morphology covers the rest of the cases.
“In the familiar form of Parkinson’s disease, α-synuclein protein is produced two to three times as much as needed, and neurons can’t get rid of it, making it more toxic and causing the disease,” says Professor Issazadeh-Navikas. Says.
“Our study investigated whether the absence of the α-synuclein protein in mice affects the development of disease in 95% of other patients. Even with this protein removed, clinical and pathology It turned out to be unaffected. Symptoms of sporadic Parkinson’s disease and a disease that mimics its pathology, “she explains.
Many preclinical studies of Parkinson’s disease have been conducted in animal models that add the α-synuclein protein or express human mutations. protein To duplicate the pathology. According to researchers, that leads to the general assumption that alpha-synuclein causes the disease, but it may not apply to most patients.
Instead, they now want to focus on the important role of interferon beta pathway signaling in sporadic Parkinson’s disease.
“Our study also considers brain inflammation and suggests that fine-tuning of interferon beta signaling, in particular, needs to be activated as a potential target for drug development. disease in the first place. At the very least, I would like to pay more attention to this and propose it as a future therapeutic target. “
The study was published in Annual Neurology Report..
Erika B. Villanueva et al, Neuron TNFα rather than α-Syn underlies PDD-like disease progression in IFNβ-KO mice, Annual Neurology Report (2021). DOI: 10.1002 / ana.26209
University of Copenhagen
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