A team of Tel Aviv University researchers claims to have made progress in the path to treating Parkinson’s disease.
The team found that a variant of a protein, caused by a genetic mutation, enhances the spread of Parkinson’s pathology through nerve cells in the brain.
“Researchers have long tried to discover how the protein α-synuclein spreads through the brain, affecting one cell after another, and gradually destroying whole sections of the brain,” said TAU doctoral student Stav Cohen Adiv Mordechai in a press release on Tuesday. “Since α-synuclein needs to cross the cell membrane in order to spread, we focused on the protein TMEM16F, a regulator situated in the cell membrane, as a possible driver of this lethal process.”
About 10 million people worldwide suffer from the brain disorder that causes unintended or uncontrollable movements, such as shaking, stiffness and difficulty with balance and coordination.
The researchers also looked for mutations or variants in the TMEM16F gene that might increase the risk for the disease.
“The incidence of Parkinson’s among Ashkenazi Jews is known to be relatively high, and the Institute conducts a vast ongoing genetic study on Ashkenazi Jews who carry genes increasing the risk for the disease,” said TAU’s Dr. Avraham Ashkenazi. “With their help, we were able to identify a specific TMEM16F mutation which is common in Ashkenazi Jews in general, and in Ashkenazi Parkinson’s patients in particular.”
The research was published in the scientific journal Aging Cell.
Earlier this year, Israeli researchers discovered a novel method to detect protein aggregation in cells—a hallmark of Parkinson’s disease—which might enable diagnosis up to 15 years before the first symptoms appear.
Although there is no cure as of yet for Parkinson’s disease, there are medications that help alleviate symptoms.
