February 26, 2025
Uncategorized

FAM171A2 Drives Parkinson’s via α-Synuclein Uptake

Unraveling a New Clue in Parkinson’s Disease: The Role of FAM171A2

Parkinson’s disease, a debilitating neurological disorder, is characterized by the buildup and spread of abnormal alpha-synuclein (α-syn) protein clumps, called fibrils, in the brain. Understanding how these fibrils spread from neuron to neuron is crucial for developing effective treatments. Exciting new research has identified a potential culprit: a gene called FAM171A2.

Here’s a breakdown of the findings:

  • FAM171A2, a Parkinson’s Risk Gene: This gene has been linked to an increased risk of developing Parkinson’s disease. The study found that higher levels of FAM171A2 actually encourage neurons to take up these harmful α-syn fibrils.
  • How FAM171A2 Works: Think of FAM171A2 like a docking station on the surface of neurons. It interacts with the tail end of α-syn fibrils, attracting them and facilitating their entry into the neuron. This interaction is surprisingly selective, with FAM171A2 binding to fibrils over 1000 times more strongly than to other forms of α-syn.
  • The Impact of FAM171A2: When researchers increased the amount of FAM171A2 in neurons, it led to more α-syn fibrils being absorbed, worsening their spread and toxic effects. Conversely, reducing FAM171A2 levels had a protective effect, suggesting that blocking this interaction could be a promising therapeutic strategy.
  • A Potential Treatment on the Horizon? The researchers identified a drug called bemcentinib that effectively blocks the interaction between FAM171A2 and α-syn fibrils. This was demonstrated in laboratory settings, including cells and mice, offering hope for a potential new treatment avenue.

What does this mean for Parkinson’s research?

This discovery provides valuable insights into the mechanisms driving Parkinson’s disease progression. By identifying FAM171A2 as a potential “receptor” for α-syn fibrils, researchers have unveiled a new target for therapeutic intervention. While further research is needed, blocking the action of FAM171A2 with drugs like bemcentinib could offer a way to slow or even halt the spread of α-syn pathology, ultimately improving the lives of those affected by this devastating disease. This research opens exciting possibilities for future Parkinson’s therapies.