CTE Blood Biomarker: New Study Offers a Clue, Not a Test

A possible blood-based clue to chronic traumatic encephalopathy (CTE) has emerged from research published in JAMA on November 13, 2026. Scientists found that a fragment of the tau protein, already studied in Alzheimer’s disease, was elevated in blood samples from people whose brains were later confirmed to have CTE. The signal was strongest in advanced disease.

The finding matters because CTE is associated with repeated head impacts and can only be definitively confirmed by examining brain tissue after death. But the study does not deliver a ready-to-use screening test. The CTE blood comparison involved only 11 autopsy-confirmed cases, and the marker did not reliably distinguish early-stage disease from healthy controls. Researchers say larger, independent studies are essential before it can be used clinically.

Why CTE remains difficult to diagnose

Chronic traumatic encephalopathy is a progressive brain disease associated with exposure to repeated head impacts. It has been studied in people who played contact sports such as American football, boxing and rugby, as well as in some military personnel and others exposed to repeated head trauma.

CTE is identified by a distinctive pattern of abnormal tau protein in the brain. During life, however, memory problems, changes in mood or behaviour, difficulty concentrating and other symptoms can overlap with many neurological and psychiatric conditions. A history of repeated head impacts may raise concern, but symptoms alone cannot confirm the disease. The US National Institutes of Health notes that definitive confirmation still requires examination of the brain after death.

This diagnostic gap affects more than individual patients. It makes it harder for researchers to identify suitable participants for clinical trials, measure whether an experimental treatment is working, or distinguish CTE from other conditions that can occur in people with a history of head injury.

The protein fragment researchers were already tracking

The new study focused on eMTBR-tau243, a fragment derived from the microtubule-binding region of tau. Tau normally helps stabilise the internal structure of nerve cells. In certain neurodegenerative diseases, abnormal forms of the protein accumulate and form aggregates inside the brain.

Alzheimer’s disease and CTE are both classified as mixed 3-repeat and 4-repeat tauopathies because they involve two forms of tau. The research team, led by scientists at Washington University School of Medicine in St. Louis and working with collaborators including the University of California, San Francisco, investigated whether eMTBR-tau243 could reflect this shared pathology beyond Alzheimer’s disease.

The clue emerged while researchers were examining samples from people with different brain diseases. One person had an unexpectedly high level of the marker despite having no Alzheimer’s pathology at autopsy. A review of the brain tissue showed advanced CTE. That observation prompted the team to examine additional samples.

What the JAMA study actually found

The case-control study included 229 participants drawn from four US biorepositories. Researchers analysed cerebrospinal fluid and plasma using a mass-spectrometry-based assay. The overall study population should not be confused with the much smaller group used for the CTE blood comparison.

For that comparison, the researchers had plasma samples from 11 people whose CTE was confirmed at autopsy and 20 cognitively unimpaired controls. Median plasma eMTBR-tau243 was 1.93 femtomoles per litre in the CTE group, compared with 0.29 femtomoles per litre among controls. The median was higher still in the 14-person Alzheimer’s disease comparison group, at 11.25 femtomoles per litre.

The results also varied by CTE stage. The marker distinguished stage III and stage IV CTE from controls with an area under the receiver operating characteristic curve of 0.97. That is a strong signal within this small sample. But for stage I CTE, the area under the curve was 0.64, with a confidence interval wide enough to show substantial uncertainty. In other words, the study did not demonstrate reliable early-stage detection.

The wider dataset also found elevated levels in Alzheimer’s disease and in a subset of people with inherited frontotemporal lobar degeneration involving mixed tau pathology. This is important scientifically, but it also points to a central limitation: eMTBR-tau243 reflects a type of tau-related brain pathology rather than uniquely identifying CTE.

Why a promising biomarker is not yet a diagnosis

A biomarker is a measurable biological signal. A diagnostic test must do more: it needs to show, in the intended patient population, that it can identify a disease reliably, distinguish it from other conditions and produce results that clinicians can interpret safely.

The new findings are preliminary for several reasons. First, the CTE blood group was small. Second, the marker performed much better for advanced disease than for stage I disease. Third, Alzheimer’s disease can also raise eMTBR-tau243, and the two conditions may coexist. A positive result by itself therefore cannot tell a clinician which disease is present.

The study also relied on samples from biorepositories, many linked to autopsy or genetic information. That makes the research valuable for connecting a blood measurement with confirmed brain pathology, but it does not establish how the marker performs in a general clinic, among living athletes with symptoms, or in people with other causes of cognitive change.

The authors conclude that further validation in larger cohorts is needed. Longitudinal studies will also be important: researchers need to know whether levels change as disease progresses, whether the marker can detect changes before advanced pathology develops, and whether it can help track response to treatment.

What could change if the findings hold up?

If future studies confirm the signal, a blood biomarker could make CTE research more practical. It might help investigators identify people who warrant closer specialist assessment, support the design of clinical trials, or provide a way to monitor biological changes during experimental treatment. It could also help researchers study people at elevated risk after years of repeated head impacts.

Washington University has licensed the technology for measuring eMTBR-tau243 in blood to C2N Diagnostics, a university startup that also developed a blood test to aid Alzheimer’s diagnosis. The CTE application, however, has not been validated for clinical diagnosis. The university’s report also discloses financial interests involving the institution and some researchers in the licensed technology, an important consideration when evaluating early-stage findings.

For now, the study should be seen as a research advance rather than a new service for athletes or former players. People concerned about symptoms after head injury should seek advice from qualified healthcare professionals; this experimental marker is not a substitute for clinical evaluation. General background on traumatic brain injury is available from the US National Institute of Neurological Disorders and Stroke.

The bigger lesson: better measurement must accompany better prevention

A test that can eventually identify CTE in living people would be valuable, but diagnosis alone would not prevent the injuries associated with it. Reducing avoidable head impacts, improving concussion recognition and ensuring that people are not pressured to return to play before recovery remain essential priorities.

The latest finding also sits within a wider expansion of brain research. World of Now recently covered an international effort to map 25.5 million cells in the basal ganglia, a brain network involved in movement, motivation and decision-making. Such atlases and emerging biomarkers address different questions, but together they show how researchers are building more precise ways to connect molecular changes with brain function and disease.

The central message is one of measured optimism. eMTBR-tau243 offers a credible new lead for studying advanced CTE, but it is not yet a validated diagnostic test. The next step is not immediate clinical adoption; it is replication, larger cohorts and careful testing of whether the signal can help patients without creating false certainty.

Frequently asked questions

Can a blood test diagnose CTE now?

No. CTE can currently be definitively confirmed only through examination of brain tissue after death. The eMTBR-tau243 finding is preliminary and has not been validated as a clinical diagnostic test for CTE.

What did the new study discover?

Researchers found higher blood levels of eMTBR-tau243 in 11 people with autopsy-confirmed CTE than in healthy controls. The signal was stronger in advanced CTE, but it did not reliably identify stage I disease.

Does a high eMTBR-tau243 result mean someone has CTE?

No. The marker is also elevated in Alzheimer’s disease and some other tau-related conditions. It cannot identify CTE on its own, and the study does not support using it for self-screening or routine diagnosis.