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New evidence challenges understanding of ʲ쾱ԲDz’s disease

Preclinical results show movement relies on a steady supply of dopamine, helping explain why current treatments work and how they could be improved
Published: 17 December 2025

A 鶹ýվ-led study is challenging a popular theory about how dopamine drives movement, a discovery that could shift how scientists think about ʲ쾱ԲDz’s disease treatments.

Published inthe research found dopamine does not set the speed or force of each movement, as had been thought. Instead, it appears to act as the underlying support system that makes movement possible.

“Our findings suggest we should rethink dopamine’s role in movement,” said senior authorNicolas Tritsch,Assistant Professor in 鶹ýվ’s Department of Psychiatry and researcher at the Douglas Research Centre. “Restoring dopamine to a normal level may be enough to improve movement. That could simplify how we think about ʲ쾱ԲDz’s treatment.”

Dopamine is known to be important for motorvigour, which is the ability to move with strength and speed. In ʲ쾱ԲDz’s patients, dopamine-producing neurons deteriorate, leading to slower movement,tremorsand balance issues.

The standard treatment for ʲ쾱ԲDz’s, Levodopa, helps restore movement, butwhyit works is not well understood. In recent years, advanced tools detected fast dopamine spikes during movement, which led many to believe these spikes controlvigour.

The new study points in the opposite direction.

“Rather than acting as a throttle that sets movement speed, dopamine appears to function more like engine oil.It’sessential for the system to run, but not the signal thatdetermineshow fast each action is executed,” said Tritsch.

Measuring dopamine in real time

The researchers measured brain activity in mice as they pressed a weighted lever, turning dopamine cells “on” or “off” using a light-based technique.

If fast dopamine bursts did controlvigour, changing dopamine at that moment should have made movements faster or slower. To their surprise, it had no effect. In tests with levodopa, they found the medication worked by boosting the brain’s baseline level of dopamine, not by restoring the fast bursts.

A more precise target for treatment

a number projected to more than double by 2050 as the population ages.

A clearer explanation for why levodopa is effective opens the door to new therapies designed tomaintainbaseline dopamine levels, the authors note.

It also encourages a fresh look at older therapies. Dopamine receptor agonists have shown promise but caused side effects because they acted too broadly in the brain. The new finding offers scientists a sense of how to design safer versions.

About the study

“” byHaixinLiu and Nicolas Tritsch et al., was published inNature Neuroscience.

The study was funded by the Canada First Research Excellence Fund, awarded through the Healthy Brains, Healthy Lives initiative at 鶹ýվ and the Fonds de Recherche du Québec.

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