For decades, Parkinson’s disease has been framed as a problem of a single patch of brain tissue that controls movement. New work suggests the condition may instead arise from a deeper, far-reaching network that links motion, thinking, mood, and even sleep. That shift in perspective could reshape how I, and many clinicians and researchers, think about diagnosing and treating Parkinson’s in the years ahead.
Rather than a localized fault, scientists now argue that Parkinson’s behaves like a disorder of a broad somato-cognitive action network, or SCAN, that knits together regions that plan actions, move muscles, and monitor the body’s internal state. If that is right, the field may be on the verge of moving from chasing symptoms at the surface to targeting the brain’s underlying wiring.
From a single spot to a somato-cognitive action network
For most of the modern era of neurology, Parkinson’s has been tied to the loss of dopamine cells in a midbrain region called the substantia nigra and to a motor loop running through the basal ganglia. That model explains the classic tremor and slowness, but it has always struggled with the full range of problems people face, from anxiety to constipation. In the new work, researchers describe Parkinson as a disorder of a somato-cognitive action network, or SCAN, that connects movement areas in the cortex with deeper structures that handle body signals and internal drives, arguing that this broader wiring pattern better matches what patients actually experience.
Scientists involved in the project say this SCAN network links regions that plan and execute actions with those that handle thinking and bodily awareness, which helps explain why symptoms can span gait freezing, memory lapses, and blood pressure swings in the same person. In interviews, Scientists described how damage in this network could cause someone who usually walks quickly to suddenly shuffle, or a person who thinks clearly to become slow and indecisive, supporting the idea that Parkinson is as much a cognitive and body-sensing disorder as a movement one.
What the new brain maps actually show
The case for SCAN as the core of Parkinson’s rests on unusually large and detailed brain maps. Earlier this year, a team led by Liu assembled brain imaging from more than 800 participants across institutions in the United States and China, comparing people with Parkinson’s to those without the disease. By stitching together structural scans, functional connectivity, and stimulation data from deep brain surgery, they traced how signals move through the SCAN and how that pattern differs in patients.
In a companion report, an analysis of those datasets showed that Parkinson is marked by excessive connectivity between the SCAN and the subcortex, a region that helps regulate movement, sleep, and body functions. The same work found that when stimulation hit parts of this network, people’s motor symptoms and related cognitive and bodily problems shifted in predictable ways, which is exactly what I would expect if the SCAN is not just correlated with Parkinson but actively driving it.
Why the SCAN model explains so many “odd” symptoms
Anyone who has spent time in a Parkinson clinic knows that the disease rarely stays in a narrow lane of tremor and stiffness. People describe losing their sense of smell, acting out dreams, struggling with depression, and feeling their thinking slow down long before a formal diagnosis. By framing Parkinson as a SCAN disorder, the new model offers a single wiring diagram that can connect these dots instead of treating each symptom as a separate add-on.
Reporting on the work highlights how The SCAN network, which links movement and thinking, could explain why a person might suddenly freeze in a doorway or feel unable to initiate a simple action even when their muscles are strong. In one account, The SCAN is described as tying together motor planning with internal predictions about the body and environment, so when the network misfires, people can experience both physical freezing and a sense that their thoughts are stuck. Coverage from NPR, By Jon Hamilton, noted that Scientists say this symptoms, including the odd feeling that the body is not responding to what the mind wants to do.
Rethinking deep brain stimulation and other treatments
If Parkinson really stems from a faulty SCAN, then the standard targets for deep brain stimulation may have been hitting the wrong parts of the circuit. For years, surgeons have aimed DBS electrodes at structures like the subthalamic nucleus and globus pallidus, with good but inconsistent results. The new work suggests that the best outcomes come when electrodes land in nodes that are strongly connected to the SCAN rather than in any single anatomical landmark.
The international team behind the new model included people with Parkinson receiving DBS as well as non-invasive therapies such as transcranial magnetic stimulation, and they found that benefits tracked how strongly the stimulated region linked into the SCAN. In one report, group included people or other stimulation, and those whose electrodes or magnets engaged the SCAN showed improvements not just in movement but in sleep problems and cognitive decline. Separate work in a high-profile journal notes that DBS efficacy has with adaptive stimulation protocols and advanced neuroimaging, but existing targets have shown limited durability, which fits the idea that the field has been stimulating pieces of a larger network without fully understanding its shape.
Global collaboration and the promise, and limits, of a new “source”
The scale and ambition of the SCAN work reflect a wider shift toward global, data-heavy neuroscience. A new international study led by China’s Changping Laboratory, in collaboration with Washington University School of Medicine in St. Louis, framed Parkinson as a network disorder and argued that future therapies should aim to fix the underlying circuitry, not just tamp down visible symptoms. In describing that effort, one release emphasized that new international study is trying to map the SCAN precisely enough that surgeons and device makers can design more targeted interventions.
Other coverage has stressed just how much this reframes the basic story of Parkinson. One feature described how Scientists discover brain that could change understanding of why the disease affects everything from walking to mood, and another piece put it bluntly that Scientists May Have, Disease by identifying the SCAN as the likely driver. A separate analysis argued that Parkinson’s May Emerge a SCAN-based fault deeper in the brain than earlier models suggested, and a follow-up noted that Parkinson, May Emerge, as summarized by Carly Cassella, Thu, with reports of a several-fold difference in response rate when stimulation targeted SCAN-linked regions. I see real promise in that, but I also read it as a reminder that the field is still early in translating these maps into reliable, everyday care for the millions of people living with Parkinson.
More from Morning Overview
*This article was researched with the help of AI, with human editors creating the final content.
