Scientists say they may have uncovered a key mechanism that allows Parkinson’s disease to spread through the brain—and identified a potential way to slow the process.

The findings, published in the journal Nature Communications, suggest that two proteins on the surface of nerve cells act as entry points for the toxic protein linked to Parkinson’s disease.

Blocking those proteins dramatically reduced disease-related damage in laboratory and animal experiments.

Parkinson’s disease is a progressive neurological disorder that affects movement, balance and coordination.

Roughly 1.1 million Americans are living with Parkinson’s disease, and nearly 90,000 people are diagnosed each year, according to the Parkinson’s Foundation.

Common symptoms include tremors, slowed movement, stiffness and balance problems.

A hallmark of the condition is the buildup of a misfolded protein called alpha-synuclein (α-synuclein), which accumulates inside brain cells and is thought to spread from neuron to neuron as the disease worsens.

While scientists have long known that alpha-synuclein appears to move through the brain, exactly how it enters healthy neurons has remained unclear.

Researchers at Yale School of Medicine set out to answer that question by screening thousands of proteins found on the surfaces of cells.

The team identified two proteins—called mGluR4 and NPDC1—that appear to work together as a receptor complex, helping misfolded alpha-synuclein bind to and enter healthy nerve cells.

Senior author Dr. Stephen Strittmatter, chair of the Department of Neuroscience at Yale School of Medicine, said drugs targeting one of the newly identified proteins could be a realistic prospect.

“Drugs targeting mGluR4 are very plausible for development,” he told Newsweek. “Some mGluR4 drugs—not specific for synuclein blockade—have already entered trials.”

While he noted that much less is known about NPDC1 and that it is not yet clear whether it can be targeted with drugs, Strittmatter said identifying medications that disrupt the alpha-synuclein pathway through mGluR4 is “quite plausible.”

To test the finding, the researchers exposed mice to alpha-synuclein fibrils, clumps of the protein that can trigger Parkinson’s-like damage.

In animals lacking both mGluR4 and NPDC1, dopamine-producing neurons were largely protected from degeneration compared with normal mice.

The results suggest that preventing alpha-synuclein from entering healthy neurons could interrupt the cycle that allows the disease to spread through the nervous system.

Strittmatter said the team’s goal was to find a treatment that could modify the disease itself rather than simply relieve symptoms.

“The design of our experiments was to search for disease modifying therapies that would slow, halt or reverse synuclein mediated damage to neurons,” he said.

Strittmatter said that if the findings can be translated into a treatment, the approach could potentially slow, stop or even reverse Parkinson’s disease and related neurological disorders driven by alpha-synuclein buildup.