The discovery of stage 1 chronic traumatic encephalopathy (CTE) in a 24-year-old former National Football League (NFL) player is drawing renewed attention to how early the brain disease may begin to develop in athletes exposed to repeated head impacts.
Researchers at the Boston University CTE Center found that former Dallas Cowboys defensive lineman Marshawn Kneeland showed pathological signs consistent with CTE during a postmortem examination conducted after he died by suicide in November.
Kneeland had stage 1 CTE, the earliest recognized stage of the progressive neurodegenerative disease linked to repetitive blows to the head.
While CTE has long been associated with retired professional athletes who spent years in contact sports, the diagnosis in such a young player highlights that disease-related changes can emerge far earlier than many people realize.
Experts caution, however, that stage 1 CTE does not necessarily mean a person experienced severe neurological symptoms during life, but reveals that the disease process may begin years before more noticeable cognitive, behavioral, or emotional changes develop.
What Is CTE?
Chronic traumatic encephalopathy is a progressive brain disease associated with repeated head impacts, including both concussions and the more frequent, lower-force blows that may not produce immediate symptoms.
Unlike a single traumatic brain injury, CTE is thought to develop over time as abnormal forms of a protein called tau accumulate in specific regions of the brain. These protein deposits interfere with normal brain function and may eventually spread to additional areas as the disease progresses.
The diagnostic criteria for CTE were established through a consensus process led by the National Institute of Neurological Disorders and Stroke. Researchers identify the disease by examining brain tissue under a microscope and looking for a distinctive pattern of abnormal tau surrounding small blood vessels at the depths of cortical folds.
What Stage 1 CTE Means
Stage 1 represents the mildest form of CTE identified through postmortem examination.
At this stage, researchers typically find one or a few isolated areas containing abnormal tau deposits. The pathology is generally limited rather than widespread throughout the brain.
Because the disease is only confirmed after death, scientists cannot definitively connect stage 1 pathology with specific symptoms experienced during life. Some individuals with early-stage CTE may have reported headaches, mood changes, or difficulties with attention, while others may have shown no obvious neurological problems at all.
This uncertainty is one reason researchers continue to study how pathological findings correspond with clinical symptoms. Not every person with early CTE pathology appears to develop dementia or severe neurological impairment.
The National Institute on Aging notes that scientists are still working to determine why some individuals develop more advanced disease while others do not.
Why CTE Can Only Be Diagnosed After Death
Despite growing public awareness, there is currently no validated clinical test capable of definitively diagnosing CTE in living patients.
Doctors may evaluate athletes for concussion, traumatic brain injury, or persistent neurological symptoms using brain imaging, neuropsychological testing, and clinical examinations. However, these methods cannot confirm the presence of the characteristic tau pathology of CTE.
Instead, diagnosis requires microscopic examination of brain tissue following death.
Researchers are actively investigating blood biomarkers, advanced PET imaging techniques, and cerebrospinal fluid testing that may eventually help detect CTE during life. While several approaches have shown promise in research settings, none has yet been validated for routine clinical diagnosis.
The National Institutes of Health continues to support studies aimed at identifying reliable biomarkers that could improve diagnosis and potentially guide future treatments.
Repetitive Head Impacts Remain the Biggest Risk Factor
Scientists emphasize that CTE is linked most strongly to cumulative exposure to repetitive head impacts rather than the number of diagnosed concussions alone.
Football players may experience hundreds or even thousands of subconcussive impacts throughout their careers. Although these hits do not cause immediate concussion symptoms, researchers believe they may contribute to long-term changes within the brain.
Studies involving former football players, military veterans, boxers, and athletes in other collision sports continue to strengthen the association between repeated head trauma and CTE pathology.
Still, researchers stress that not everyone exposed to repetitive head impacts develops CTE. Genetic factors, duration of exposure, age at first participation, and other biological variables may influence individual risk, though many questions remain unanswered.
The Centers for Disease Control and Prevention recommends proper concussion management, adherence to safety rules, and limiting unnecessary head impacts as important strategies for reducing brain injury risk.
A Young Diagnosis Raises New Questions
The reported diagnosis in Kneeland adds to a growing body of evidence suggesting that pathological changes associated with CTE can emerge much earlier than previously recognized.
Over the past decade, researchers have identified early-stage CTE in some younger athletes who participated in contact sports at the high school, collegiate, and professional levels. These findings have fueled ongoing discussions about athlete safety, return-to-play protocols and ways to reduce repetitive head impacts without eliminating participation in sports altogether.
Scientists caution against drawing broad conclusions from any single case. Individual diagnoses help researchers understand the disease but cannot predict how CTE develops across the wider athletic population.
Instead, experts say each confirmed case contributes valuable information that may improve future prevention efforts and, eventually, the development of tests capable of identifying the disease before irreversible brain damage occurs.
