Prof. Uri Ashery and Dr. Dana Bar-on.
(photo credit: TEL AVIV UNIVERSITY)
New research by a team of scientists at Tel Aviv University could significantly delay the progression of Parkinson’s disease.
Specifically, the researchers unveiled a novel method for detecting the aggregation of the protein alpha-synuclein, a hallmark of the neurodegenerative disorder that causes a debilitating decrease in a patient’s motor and non-motor functions. While therapies exist to alleviate some symptoms of the disease, there is no cure.
There are close to one million Americans and 10 million people around the world affected by the disease. People die with Parkinson’s, not from; as symptoms worsen, they can cause incidents that result in death.
Parkinson’s affects predominantly dopamine-producing neurons in a specific area of the brain called substantia nigra. Symptoms generally develop slowly over years. As such, according to TAU, by the time a patient is diagnosed with Parkinson’s disease, 50% to 80% of these cells in that part of the brain are already dead, possibly due to development of toxicity as result of alpha-synuclein aggregation.
The researchers have developed a new method for tracking early stages of aggregation of alpha-synuclein using super-resolution microscopy and advanced analysis, explained Prof. Uri Ashery, co-author of the study and head of TAU’s Sagol School of Neuroscience and TAU’s George S. Wise Faculty of Life Sciences.
“Together with our collaborators at Cambridge University, who developed a special mouse model for Parkinson’s disease, we were able to detect different stages of the aggregation of this protein,” he said in a release. “We correlated the aggregation with the deteriorating loss of neuronal activity and deficits in the behavior of the mice.”
The co-author of the study, Dr. Dana Bar-On of the Sagol School of Neuroscience, said that by being able to detect early stages of alpha-synuclein aggregation, doctors will be able to monitor the effects of drugs on this aggregation.
Working with the Max Planck Institute in Gottingen and Ludwig-Maximilians-Universität München, the researchers were already able to demonstrate the effect of the drug, anle138b, on this protein aggregation. They, likewise, correlated those results with the normalization of the Parkinson’s phenotype in the mice.
The research was published June 5 in the Acta Neuropathologica medical journal.
“This is a significant step forward in the world of Parkinson’s research,” Ashery said, adding that “by detecting aggregates using minimally invasive methods in relatives of Parkinson’s disease patients, we can provide early detection and intervention and the opportunity to track and treat the disease before symptoms are even detected.”
What’s next? Bar-On said that the team is currently working to implement the methods in a minimally invasive manner with Parkinson’s patients.
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