The honest answer is that no one knows exactly how common CTE is in the general population, because the disease can only be definitively diagnosed after death through brain autopsy. What researchers do know comes from brain bank studies, where families donate the brains of deceased individuals for examination. These studies reveal striking numbers in certain groups, but they come with important caveats about who gets studied in the first place.
CTE Rates in Professional Football Players
The most widely cited figure comes from Boston University’s CTE Center, which has diagnosed CTE in 345 of 376 former NFL players whose brains were donated for study. That’s 91.7%. But that number doesn’t mean 9 out of 10 NFL players will develop CTE. Brain banks receive donations from families who suspected something was wrong, meaning the sample is heavily skewed toward people who were already showing symptoms. Players who lived healthy lives into old age are far less likely to have their brains donated for CTE research.
The true prevalence among all current and former NFL players remains unknown. What the brain bank data does confirm is that CTE is not rare among professional football players, and that it occurs at rates far exceeding anything seen in the general population.
Young and Amateur Athletes Are Affected Too
CTE isn’t limited to professionals who played for decades. An NIH-funded study examined 152 brains from contact sport players who died before age 30. More than 40% of them (63 out of 152) had CTE. Critically, over 70% of those diagnosed with CTE had only played at the amateur level, meaning high school or college sports. This finding shifted the conversation from “how many years in the NFL” to “how many hits to the head, period.”
How Years of Play Affect Risk
Research from Boston University found that the odds of developing CTE double for roughly every 2.6 additional years of football played. Each extra year on the field increased the odds of having CTE by about 30%, and increased the odds of having severe rather than mild CTE by about 14% per year.
Importantly, the number of diagnosed concussions doesn’t appear to drive CTE risk. What matters is the total accumulation of head impacts, including the routine, smaller hits that happen on every play. For every additional 1,000 estimated head impacts over a career, the odds of CTE rose by 21%. Among those who already had CTE, every additional 1,000 impacts increased the odds of severe disease by 13%. This means linemen who absorb hundreds of subconcussive hits per season may face higher risk than skill players who suffer a few dramatic concussions.
CTE in Military Veterans
Military personnel, particularly those exposed to blasts or physical head trauma during service, also show elevated rates. A study published in the New England Journal of Medicine examined brains from veterans with and without blast exposure. Among 45 brains from veterans with blast exposure histories, 3 had CTE. That rate was roughly 1.7 times higher than in veterans without blast exposure, though the sample was too small to be statistically definitive. Veterans who sustained head injuries from physical impact (the head striking an object, separate from blast) had about four times the risk compared to those without such injuries.
What About the General Population?
Studies applying CTE diagnostic criteria to people without known histories of repetitive head trauma have produced wildly inconsistent results, ranging from 0% to 35% depending on the study. Some research has even identified CTE-like changes in people with a single traumatic brain injury or no documented head trauma at all. This variability reflects how new and unsettled the diagnostic criteria still are, and why pinning down a baseline rate in the general population has proven so difficult.
Among people with no significant history of contact sports or head trauma, CTE appears to be uncommon to rare. But the exact number remains a gap in the science.
How CTE Progresses
CTE is classified into four stages based on how extensively abnormal tau protein has spread through the brain. In Stage I, only one or two small clusters of damaged tissue appear, typically in the frontal lobe. By Stage II, three or more clusters are present across multiple brain regions. Stage III brings visible brain shrinkage and enlarged ventricles, with damage spreading into memory-critical structures like the hippocampus. Stage IV involves widespread degeneration throughout the brain, including areas controlling movement, along with significant tissue loss in the frontal and temporal lobes.
Symptoms tend to follow two patterns. One form appears in the late 20s to early 30s and primarily involves behavioral and mental health changes: depression, anxiety, impulsive behavior, and aggression. The other form emerges later, around age 60, and centers on memory and thinking problems that can progress to dementia. Some people experience elements of both.
Why CTE Is Still So Hard to Count
The central problem is that CTE cannot yet be diagnosed in a living person. Researchers have explored tau PET scans, which can detect the abnormal protein deposits that characterize the disease. Studies show former elite football players have higher signals in the frontal, parietal, and temporal brain regions, but results vary considerably between individuals and don’t consistently match clinical symptoms. When compared against autopsy findings, these scans show only modest accuracy, potentially useful for advanced-stage CTE but insufficient as a standalone diagnostic tool.
Blood tests for Alzheimer’s-related proteins have become increasingly available, but the tau tangles in CTE are structurally different from those in Alzheimer’s, so these tests don’t reliably detect CTE. Their main value right now is helping rule out Alzheimer’s in someone with a history of head impacts who is experiencing cognitive decline.
Until a reliable living diagnostic test exists, prevalence estimates will remain tethered to brain bank data with all its selection bias. The numbers we have almost certainly overestimate rates in the broader population of people who played contact sports, while simultaneously underestimating the total number of affected individuals who were never tested.
Beyond Contact Sports
Emerging reports suggest CTE may also affect survivors of long-term domestic violence, though the research is still in its earliest stages. The first publicly documented case involved a 69-year-old woman who endured decades of physical abuse and developed memory problems in her mid-40s. Her autopsy revealed severe CTE alongside Alzheimer’s disease. Only a handful of similar cases exist in the scientific literature so far, but they point to repetitive head trauma from any source, not just sports or military service, as a potential cause.