JERUSALEM, Nov. 12 (Xinhua) -- Israeli researchers have found a variation of a key protein in the body that may speed up the spread of Parkinson's disease in brain cells, Tel Aviv University (TAU) announced on Tuesday.
TAU explained that this protein could be targeted to develop effective treatments for Parkinson's disease, which affects nearly 10 million people worldwide.
Parkinson's disease progresses as a protein called alpha-synuclein builds up in brain cells, eventually causing cell death.
In a new study published in the journal Aging Cell, TAU researchers looked at how this harmful alpha-synuclein protein spreads through the brain, damaging more areas over time.
Since alpha-synuclein needs to cross cell membranes to spread, the team studied TMEM16F, a membrane protein regulator, as a possible driver of this process.
Using genetically modified mice, the researchers found that deleting the TMEM16F gene reduced the spread of alpha-synuclein to nearby healthy cells, compared to its spread from normal cells.
They then identified a specific mutation in TMEM16F common among Parkinson's patients and found that cells with this mutation released more harmful alpha-synuclein than those with the normal gene.
According to the researchers, this mutation increases TMEM16F activity, which impacts how cells release substances from their membranes. The faulty alpha-synuclein is then picked up by nearby healthy brain cells, leading to protein clumps that gradually spread, damaging more brain cells.
"If we can block TMEM16F to stop or reduce the release of harmful alpha-synuclein from brain cells, we might slow or even halt the spread of Parkinson's disease in the brain," the researchers concluded. ■
