“All of the mice we treated showed dramatic improvement in their motor skills. The results exceeded our expectations and suggest that, after further study, this therapeutic approach could slow the progression of Parkinson’s in humans,” says Double.

But experts caution that Parkinson’s is a complex condition that will likely require multiple combined interventions. A single treatment may have limited effect, but its efficacy may be enhanced by integrating it with other therapeutic approaches.

In that context, Double’s team’s findings could be complemented by recent research from Stanford University focused on restoring communication between neurons in a subtype of Parkinson’s linked to mutations in the gene responsible for producing an enzyme called LRRK2.

In these cases, the mutation causes hyperactivity of the enzyme, altering the structure of brain cells and disrupting signaling between dopaminergic neurons and those in the striatum, a deep brain region related to movement, motivation, and decision-making.

It is estimated that about 25 percent of Parkinson’s cases are genetic in origin, and the LRRK2 mutation is one of the most frequent. The team led by Stanford neuroscientist Suzanne Pfeffer proposed that inhibiting the excessive activity of this enzyme could stabilize symptoms, especially if detected in early stages. The goal was to regenerate primary cilia, antenna-like structures that enable communication between cells.

The hypothesis was tested in mice genetically modified to exhibit LRRK2 hyperactivity and early symptoms of the disorder. For two weeks, these animals were administered with a compound called MLi-2, which binds to the enzyme and reduces its activity.

In this first test, no relevant changes were observed, which the researchers attributed to the fact that the examined neurons and glia—another type of cell in the nervous system, which support neurons—were already mature and were not in the cell division phase.

However, a review of the scientific l...