31/12/2025
Scientists Say a Major Assumption About
Parkinson’s Disease May Be Wrong
A new study suggests dopamine may not directly
control how fast or forcefully movements are
made, challenging a long-standing view in
neuroscience.
New research led by McGill University is
questioning a widely held idea about how
dopamine influences movement, a finding that
may change how scientists approach treatments
for Parkinson’s disease.
The study, published in Nature Neuroscience,
shows that dopamine does not directly control
the speed or strength of individual movements,
contrary to previous assumptions. Rather, the
chemical appears to provide the essential
background conditions that allow movement to
happen in the first place.
“Our findings suggest we should rethink
dopamine’s role in movement,” said senior
author Nicolas Tritsch, Assistant Professor in
McGill’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 Parkinson’s
treatment.”
Dopamine plays a key role in motor vigor, or
the ability to move quickly and with force. In
people with Parkinson’s disease, the gradual
loss of dopamine-producing neurons leads to
slowed motion, tremors, and problems with
balance.
Levodopa is the most commonly used medication
for Parkinson’s disease and can improve a
patient’s ability to move, yet scientists
still do not fully understand the mechanism
behind its benefits. More recently, sensitive
technologies have picked up rapid dopamine
surges that occur during movement, prompting
many researchers to suspect these brief spikes
help determine motor vigor.
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’s essential for the
system to run, but not the signal that
determines how 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 control vigor,
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
More than 110,000 Canadians live with
Parkinson’s disease, 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 to maintain baseline 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.
