In a stunning advancement for neurodegenerative research, scientists at Stanford Medicine have revealed a discovery that could dramatically reshape how we understand and potentially treat Parkinson’s Disease. At the heart of this breakthrough is a single enzyme known as LRRK2.
When overactive, LRRK2 interferes with the brain’s dopamine-producing neurons, disrupting movement and motivation – core symptoms of Parkinson’s. But researchers have found that by using a compound called MLi-2 to inhibit LRRK2 activity in mice, damaged neurons were able to regrow essential structures called cilia, which serve as cellular communication hubs.
Three months of treatment led to a stunning transformation: the once-impaired neurons began functioning like healthy ones again. Not only was dopamine signaling restored, but cellular architecture improved, offering a real possibility that early intervention could not just slow but reverse the progression of Parkinson’s.
And the promise doesn’t stop there.
Since heightened LRRK2 activity is also present in other forms of Parkinson’s – and possibly in other brain disorders – this enzyme-blocking strategy may pave the way for broader therapies targeting multiple neurodegenerative diseases.
The study, published July 1, 2025 in Science Signaling and led by Dr. Suzanne Pfeffer, reflects an international collaboration of experts determined to push the boundaries of brain science.
This isn’t just another piece of lab research. It’s a paradigm-shifting development for millions worldwide living with Parkinson’s and searching for new answers.