Ever wondered how Parkinson’s disease spreads within the brain? A key culprit is the build-up and movement of abnormal alpha-synuclein (α-syn) protein clumps, called fibrils. A recent study sheds light on this process, uncovering a potential new therapeutic target. Here’s the breakdown:

• A gene called FAM171A2 may play a significant role in Parkinson’s development. This gene increases the risk of Parkinson’s by encouraging brain cells to absorb these harmful α-syn fibrils.
• Higher levels of FAM171A2 worsen the spread and toxic effects of α-syn. Like a doorway letting in unwanted guests, more FAM171A2 allows more α-syn fibrils to enter brain cells, causing further damage.
• Reducing FAM171A2 levels in neurons has a protective effect. This suggests that blocking FAM171A2 could help slow or stop the progression of Parkinson’s.
• How does FAM171A2 work? The outer part of the FAM171A2 protein attaches to the tail end of the α-syn fibril through electrical attraction. Importantly, it’s over 1000 times more attracted to the harmful fibrils than to the normal α-syn protein.
• There’s a potential drug that could block this interaction. Bemcentinib, a drug already being researched, has shown promise in blocking the binding of FAM171A2 to α-syn fibrils in lab tests and even in mice.

This research is a big step towards understanding how Parkinson’s spreads and offers hope for new treatments. By targeting FAM171A2, we may be able to prevent the uptake of toxic α-syn fibrils and protect brain cells from further damage. While more research is needed, this discovery paves the way for potential therapies that could change the course of Parkinson’s disease.