The moment is unremarkable: a player rises, meets the ball with their forehead, and drops back to the pitch. No collision, no concussion, no stoppage of play. Just a header — one of thousands a soccer player might execute across a career.
But a new study suggests something measurable is happening beneath the surface. That single, ordinary impact may be enough to release proteins into the bloodstream that scientists associate with brain cell damage and Alzheimer’s disease. What that biochemical signal actually means for players is a question researchers are only beginning to ask.
What the Study Found
Researchers at Amsterdam University Medical Center tracked 302 amateur male soccer players in the Netherlands across 11 matches. Blood was drawn before each game, immediately after, and again 24 to 48 hours later. Cameras recorded how often each player headed the ball and estimated the force of each impact.
The results, published May 18 in JAMA Neurology, were unambiguous on one point: even a single header was enough to raise S100B levels in blood drawn right after a match. Players who headed the ball more than twice — or who made several high-impact headers — also showed elevated p-tau217 immediately following play.
Both proteins returned to baseline within 24 to 48 hours. The researchers note, though, that a return to baseline does not rule out lasting harm. The signal may be brief, but what it represents could be something else entirely.
Why These Two Proteins Matter
S100B is produced by astrocytes, the star-shaped support cells that help maintain the brain’s environment. Clinicians already use it as a standard marker for traumatic brain injury — it typically rises within one hour of a TBI. Seeing it elevate after an ordinary, unconcussive header is what makes the finding notable.
P-tau217 tells a different story. Tau is a protein that normally stabilizes the internal scaffolding of neurons. When the brain experiences mechanical stress, tau detaches from that scaffolding and enzymes convert it into phosphorylated forms — including p-tau217, currently one of the most reliable blood-based biomarkers used to detect Alzheimer’s disease.
The elevations observed in the study did not cross clinical diagnostic thresholds. Those thresholds, however, are calibrated to catch severe injuries — concussions, dementia — not subtle, repeated disruptions that may accumulate quietly over years.
How a Header Might Injure the Brain
The exact biological mechanism behind these biomarker rises is still unknown. Lead co-author Marsh Königs suggests the rapid acceleration and deceleration of the head during a header may produce a small-scale, concussion-like effect — not severe enough to cause symptoms, but enough to disturb brain tissue at the cellular level.
A separate study published in April 2025 supports that idea, showing that ball-to-head contact sends a pressure wave traveling through the skull. That wave has to go somewhere. Multiple pathways may be operating at once, and researchers have not yet isolated which one drives the protein release.
What they do know is that the effects appear real and measurable. A 2025 study on soccer and football players found that years of repeated head trauma kill neurons and trigger brain inflammation — pointing to potentially significant downstream consequences from these small, repeated events.
The Cumulative Concern
No single header is likely to cause lasting neurological damage on its own. The concern researchers raise is about repetition — hundreds or thousands of headers across a playing career, each producing a small biochemical response that may never fully disappear.
“These cutoffs are mostly designed to detect much more serious injuries, such as severe brain injuries or dementia,” Königs told Live Science, referring to the clinical thresholds his team’s results did not exceed. His concern centers on what happens when sub-threshold events stack up over time.
Samantha Bureau of the Concussion Legacy Foundation Canada, who was not involved in the study, echoed that concern, noting that long-term consequences are harder to track because symptoms can emerge years after exposure. “The evidence we have so far suggests that brain damage is occurring from heading soccer balls, both short and long-term,” she said. Königs also believes that running the same study with elite professional players — who head the ball more frequently and with greater force — would likely produce even more pronounced biomarker responses.
What Governing Bodies Are Doing — and What Remains Unknown
Some soccer organizations are already responding. England’s Football Association, for example, has moved to reduce permitted practice loads for headers. The policy direction is clear, even if the scientific foundation for it is still incomplete.
Peter Theobald, a medical engineer at Cardiff University who specializes in brain biomechanics, described the Dutch study as relatively strong — particularly because it included athletes from non-contact sports as a control group, which strengthens the case that heading, specifically, is driving the changes. He did note one meaningful limitation: the study did not track the same players across a full season, which would have revealed whether biomarker levels accumulate over time rather than simply resetting after each match.
That question — whether repeated sub-threshold events leave a lasting biological trace — is likely where research heads next. Right now, no scientifically established safe level of heading exists. Until one does, coaches, players, and policymakers are making decisions without a clear evidence-based threshold. The Dutch study does not resolve that uncertainty, but it sharpens the question considerably.