There’s something deeply frustrating about Parkinson’s disease. By the time your hands start shaking or your movements become stiff, half of the brain cells responsible for controlling those movements are already dead. Sometimes up to 80 percent are gone. It’s like getting a fire alarm that only goes off after your house has burned down.
But researchers from Chalmers University of Technology in Sweden and Oslo University Hospital just found something remarkable. They’ve identified biological markers that show up in the blood during the earliest stages of Parkinson’s, before the brain takes a beating. The catch? These markers only stick around for a short window.
The implications are massive. We’re talking about potentially diagnosing a disease that affects over 10 million people worldwide before it causes irreversible damage. And with aging populations, that number is expected to more than double by 2050. Right now, there’s no cure and no screening method that catches it early enough to make a real difference.
The 20-Year Silent Phase
Here’s what makes Parkinson’s so tricky. The disease moves slowly, like a glacier. For many patients, there’s an early phase that can last up to 20 years before those classic motor symptoms fully kick in. Twenty years. During all that time, changes are happening inside cells, quietly destroying the machinery that keeps your movement smooth and controlled.
Danish Anwer, a doctoral student at Chalmers and the study’s first author, put it bluntly. “By the time the motor symptoms of Parkinson’s disease appear, 50 to 80 per cent of the relevant brain cells are often already damaged or gone.”
The research team focused on two cellular processes that seem to be involved early on. One is DNA damage repair, basically your cells’ maintenance crew that fixes genetic damage. The other is the cellular stress response, which is like an emergency protocol where cells shift energy away from routine operations toward survival and repair.
Machine Learning Spots the Pattern
Using machine learning and advanced analytical methods, the team found a distinct pattern of gene activity related to DNA repair and stress response. But here’s where it gets interesting. This pattern only appeared in people in the early phase of Parkinson’s. It wasn’t there in healthy people, and it also wasn’t there in patients who already had motor symptoms.
Think about that for a second. The biological signature shows up, does its thing, and then disappears as the disease progresses. It’s like the disease leaves a temporary calling card.
“This means that we have found an important window of opportunity in which the disease can be detected before motor symptoms caused by nerve damage in the brain appear,” says Annikka Polster, Assistant Professor at Chalmers who led the study. The fact that these patterns vanish later also makes them interesting targets for future treatments focused on science and understanding early disease mechanisms.
Blood Tests vs. Everything Else
Scientists have been hunting for early Parkinson’s indicators for years. Brain imaging, spinal fluid analysis, you name it. None of them has produced a validated screening test that works before symptoms begin. They’re either too expensive, too invasive, or just not practical for widespread use.
Blood tests are different. They’re cheap, accessible, and people are already used to getting them. No special equipment needed, no spinal taps, no fancy brain scans.
“In our study, we highlighted biomarkers that likely reflect some of the early biology of the disease and showed they can be measured in blood,” Polster explains. “This paves the way for broad screening tests via blood samples: a cost-effective, easily accessible method.”
The team estimates that within five years, these blood tests could start being tested in actual healthcare settings. That’s not a guarantee they’ll work at scale, but it’s a realistic timeline for moving from lab to clinic. And long term, this research might help develop treatments that slow or even prevent the disease from progressing, incorporating advances in technology and medical diagnostics.
Drug Repurposing on the Table
One particularly interesting angle is drug repurposing. If researchers can nail down exactly how these early mechanisms work, they might be able to use drugs that were developed for completely different diseases but affect the same gene activities or cellular pathways.
“If we can study the mechanisms as they happen, it could provide important keys to understanding how they can be stopped and which drugs might be effective,” says Polster. “This may involve new drugs, but also drug repurposing, where we can use drugs developed for diseases other than Parkinson’s because the same gene activities or mechanisms are active.”
It’s a pragmatic approach that could speed up treatment development significantly. Instead of starting from scratch with new compounds, you’re working with drugs that already have safety profiles and regulatory approval for other conditions.
The study, published in npj Parkinson’s Disease, represents a significant step forward in understanding when and how Parkinson’s begins its silent assault on the brain. The research was funded by several organizations including the Michael J Fox Foundation and the Swedish Research Council, highlighting the international effort to crack this problem.
What strikes me most about this research is the cruel timing of it all. You have biological markers screaming that something’s wrong, but they only show up during a window when most people would never think to get tested because they feel completely fine. The question now is whether we can turn this scientific discovery into something that actually changes lives before it’s too late.
