How Many Balls Can Your Mind Juggle? Scientists Say Just One

Parkinson’s: Possible Clue Into Movement Disorders Like, Others

August 20, 2025 – In a promising development for neuroscience and neurodegenerative disease research, scientists have uncovered a new clue that may help explain how movement disorders such as Parkinson’s disease disrupt the brain’s ability to coordinate motion. The discovery, which centers on how the brain predicts and processes movement, could one day lead to earlier diagnoses or more targeted therapies for Parkinson’s and similar conditions.

Researchers at the University of California, San Diego, in collaboration with colleagues at the Max Planck Institute for Brain Research, have identified a potential neural mechanism that may underlie the motor impairments seen in Parkinson’s disease, Huntington’s disease, dystonia, and other movement disorders.

Their findings, published this week in Nature Neuroscience, suggest that the brain’s internal “movement prediction system” — a key component in smooth, coordinated physical activity — may be compromised in individuals with these disorders.

Predicting Before Acting

Under normal conditions, the brain doesn’t just react to movement; it predicts it. Before a person lifts a hand or takes a step, specific brain regions simulate the action internally, anticipating how the body will move and how the environment will respond. This predictive process enables fluid, precise movements and helps compensate for minor delays in feedback from muscles or senses.

In the new study, researchers used a combination of high-resolution brain imaging, electrophysiology, and behavioral testing in both healthy subjects and individuals with early-stage Parkinson’s disease. They found that a specific neural circuit involving the basal ganglia — a group of structures deep within the brain associated with motor control — showed markedly different activity patterns in those with Parkinson’s, even before symptoms were fully evident.

“The brain’s ability to simulate and predict movement appears to degrade before we see major motor symptoms,” said lead author Dr. Alina Verhoeven, a neurologist and neuroscientist at UC San Diego. “This suggests we may be able to identify and perhaps intervene earlier than we currently do.”

A Window Into the Basal Ganglia

The basal ganglia have long been implicated in movement disorders, particularly Parkinson’s, where dopamine-producing neurons that interact with these circuits are progressively lost. But this study goes further, showing how the timing and synchronization of internal movement simulations break down — and how that breakdown may explain hallmark symptoms like tremors, rigidity, and slowed motion.

Participants with early-stage Parkinson’s struggled not only with actual movement but also with imagined movement tasks, such as mentally rehearsing a hand gesture or visualizing a path through a maze. Their brain activity, recorded via EEG and fMRI, showed diminished coordination in predictive regions compared to healthy controls.

“This doesn’t mean they couldn’t imagine moving,” said co-author Dr. Ingo Lutz of the Max Planck Institute. “But the neural signals that normally prepare and align the body for action were disrupted — like an orchestra with no conductor.”

Hope for Diagnosis and Therapy

The implications are twofold: first, this predictive failure might serve as an early biomarker for movement disorders — detectable even before classic symptoms arise. Second, it points to new therapeutic targets.

“If we can strengthen or retrain these internal prediction mechanisms through neurostimulation, targeted therapy, or even virtual reality training, we may be able to slow disease progression or improve quality of life,” said Dr. Verhoeven.

While more research is needed, the findings open a new line of investigation that blends cognitive neuroscience with clinical neurology — emphasizing the role of mental simulation and internal timing in motor function.

Moving Forward

Parkinson’s disease affects more than 10 million people worldwide. Current treatments focus on replacing lost dopamine or mitigating symptoms, but do not stop the underlying neural degeneration.

“This research helps shift the focus from just treating symptoms to understanding the deeper brain dysfunctions behind them,” said Dr. Lutz. “It’s a small step, but one in the right direction.”

As scientists continue to map the intricate relationship between brain prediction and movement, studies like this one bring hope that new diagnostics — and eventually new treatments — are within reach.

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