Heading the ball: Why sports stars face dementia risk decades later

The moment a soccer player leaps and connects with the ball—that familiar rush of power and precision—carries a hidden cost that may not appear until decades later. Professional athletes who spend their careers heading balls face a starkly elevated risk of developing dementia, Alzheimer's disease, Parkinson's, and motor neurone disease. The evidence, once confined to boxing, now extends across multiple sports, and the mechanism is becoming clearer: repeated impacts cause the brain to ricochet inside the skull, damaging the delicate neural pathways that sustain cognition and motor control.

The connection between head trauma and brain degeneration is not new. In 1928, a US pathologist named Harrison Martland documented what boxers called "punch drunk"—a condition marked by confusion and an unsteady gait that sometimes progressed to dementia. For nearly a century, the problem seemed specific to boxing. That changed in the early 2000s. Jeff Astle, who played for West Bromwich Albion and England, died at 59 from early-onset dementia. An examination of his brain revealed chronic traumatic encephalopathy, or CTE—a degenerative condition characterized by abnormal protein tangles called tau. Around the same time, American football player Mike Webster died at 50 after cognitive decline and Parkinson's-like symptoms. His brain, too, showed CTE. In 2011, former Chicago Bears player David Duerson died by suicide following depression; his brain autopsy confirmed the same diagnosis.

The scale of the problem became apparent through systematic research. In 2023, Ann McKee, a neurology professor at Boston University, analyzed the brains of 376 former NFL players who had donated their bodies to science. Nearly 92 percent had CTE. The sample likely skews toward those who suspected they had the condition, but the finding is sobering. The general population carries CTE in less than 1 percent of cases. Willie Stewart, a neuropathologist at the University of Glasgow, conducted a larger epidemiological study comparing nearly 8,000 Scottish former professional footballers to 23,000 matched members of the general population. His results showed that former footballers were five times more likely to develop Alzheimer's disease, four times more likely to suffer motor neurone disease, and twice as likely to develop Parkinson's disease. Overall, they faced a 3.5-fold higher risk of dying from neurodegenerative disease. The risk was highest among defenders—players who head the ball most frequently—and increased with career length, ranging from a doubling of risk for the shortest careers to a five-fold increase for the longest.

Understanding why heading causes this damage required looking inside the living brain. Michael Lipton, a radiologist at Columbia University, used MRI scans to study young amateur soccer players, some heading the ball thousands of times per year and others not at all. Players who headed frequently performed worse on learning and memory tests and showed clear damage in the orbitofrontal cortex, the region just above the eye sockets. The white matter in this area—the brain's "network cabling" composed of fine filaments called axons—appeared particularly vulnerable. When a head impacts a ball, the force causes the brain to shift suddenly inside the skull. Because the brain has the consistency of gelatin, it compresses, twists, and deforms, straining the axons and disrupting their connections. The damage concentrates at the boundary between white and grey matter, where the two tissue types have different densities and move at different speeds during impact. Players heading more than 1,000 balls annually showed significantly greater damage in this zone.

What remains unknown is whether this early damage inevitably leads to disease. Lipton's research shows that young, healthy headers exhibit measurable brain changes without yet showing symptoms of degeneration. Some may eventually develop CTE, Alzheimer's, Parkinson's, or motor neurone disease; others may not. Genetics and lifestyle factors may determine vulnerability. One hypothesis suggests that repeated impacts damage blood vessels or trigger chronic inflammation that persists and eventually causes neurodegeneration. Another proposes that injured neurons simply degenerate over time, compounding the damage.

Protective measures are emerging, though none offers complete prevention. Researchers at Stanford University have designed American football helmets with built-in liquid shock absorbers that reduce head impact by roughly 30 percent. In the United Kingdom, following Stewart's research, heading has been removed from youth-level football. His team has also successfully campaigned to reduce heading during training sessions—a significant change, since Stewart found that professional players might head the ball 70,000 times in a career, with only a few thousand occurring in matches. The remaining 68,000 impacts happen during practice, largely unmonitored. Stewart acknowledges the fundamental tension: the risk would disappear if people stopped heading the ball entirely, but convincing athletes and sports organizations to abandon a core skill remains impractical. For now, the focus is on harm reduction—protecting young players before damage accumulates, and managing the risk for those already exposed.