Somewhere in the long human struggle to understand the injuries we inflict on ourselves in pursuit of glory and play, researchers at Washington University in St Louis have located a faint signal in the blood that may one day speak for a brain that cannot yet be examined. Chronic traumatic encephalopathy, a degeneration born of repeated blows to the head, has so far revealed itself only to the autopsy table, long after the athlete who carried it has gone. This protein fragment, eMTBR-tau243, rises with the severity of the disease, and it offers a hope that the damage might be named while a pers
Blood Test Shows Promise for Diagnosing CTE in Living Patients, Though Not Yet Validated
CTE can be diagnosed only after death, by examining brain tissue.
Why does a blood test matter so much for CTE?
Because right now the only way to confirm it is to examine brain tissue after death. Players, families and doctors have had no way to know while the person is alive.
What exactly did the researchers find?
A protein fragment, eMTBR-tau243, was higher in the blood of 11 people with autopsy-confirmed CTE than in healthy people, and it rose with how severe the disease was.
Eleven is a very small group, though. I'd keep that in front of everything else.
Fair, and the test hasn't been validated for CTE diagnosis. The authors say so.
Does it catch the disease early?
No. It distinguished advanced CTE well but could not reliably identify early-stage cases.
Which is the stage where a diagnosis would be most useful for an athlete still playing. That gap is unresolved.
So how would it be used?
Sato said it won't stand alone. Someone with repeated head injuries who tests negative for Alzheimer's but positive on this marker might have CTE.
Note the word "might." The reporting supports a clue, not a diagnosis.
Le Pouls
- A marker found in blood now offers a glimmer of hope where only autopsy once gave answers about CTE.
- The test reliably separates advanced CTE from healthy brains, but it cannot yet catch the early disease that matters most for prevention.
- Scientists are cautiously weighing whether an Alzheimer's marker can be repurposed, with the study's own authors warning it is not a standalone test.
- The sample of just 11 confirmed patients means the finding must survive larger studies before clinicians or drug trials can rely on it.
- Across American football, rugby and boxing, living and deceased athletes continue to press the question of who is harmed and who will be held to account.
Somewhere in the long human struggle to understand the injuries we inflict on ourselves in pursuit of glory and play, researchers at Washington University in St Louis have located a faint signal in the blood that may one day speak for a brain that cannot yet be examined. Chronic traumatic encephalopathy, a degeneration born of repeated blows to the head, has so far revealed itself only to the autopsy table, long after the athlete who carried it has gone. This protein fragment, eMTBR-tau243, rises with the severity of the disease, and it offers a hope that the damage might be named while a person still lives to act on the knowledge. Its promise remains provisional, since it reads advanced disease well but has not yet been proven for this purpose.
At Washington University School of Medicine in St Louis, researchers have identified a protein fragment in the blood, called eMTBR-tau243, that may someday help doctors recognise chronic traumatic encephalopathy in living people. The finding, published in JAMA Neurology, is an early step rather than a finished tool.
CTE arises from repeated head trauma and is most common in contact sports such as American football, rugby and football. Today it can only be confirmed after death, by examining brain tissue. The fragment was already known to rise in Alzheimer's disease and in other conditions marked by similar toxic protein buildup. Blood from 11 people with autopsy-confirmed CTE showed higher levels than in healthy people, and the levels climbed with disease severity.
The limits are clear. The test separated advanced CTE from healthy controls well, but it could not reliably detect early disease, the sample was small, and it has not been validated for CTE. Kanta Horie, a co-senior author, spoke of opening a new door for living patients, while Chihiro Sato urged caution: the marker is not standalone, but a positive result alongside a history of repeated head injury and a negative Alzheimer's test might point toward CTE.
The research arrives amid mounting alarm. In one study of nearly 400 donated NFL brains, 93.5% showed CTE, and more than 350 former NFL players have been diagnosed posthumously. In rugby, living former players face legal action over traumatic encephalopathy syndrome. The next test is validation: whether larger studies confirm the marker and whether it can ever reach the early stages where it is needed most.
At Washington University School of Medicine in St Louis, researchers have found a protein fragment in the blood that may eventually let doctors identify chronic traumatic encephalopathy in people who are still alive. The fragment is called eMTBR-tau243, and the finding, published in the journal JAMA Neurology, is an early step rather than a finished test.
The problem it addresses is a stubborn one. CTE is caused by repeated trauma to the head and is especially prevalent in collision and contact sports, among them American football, rugby and football. As things stand, it can be diagnosed only after death, by examining brain tissue.
The St Louis team noted that eMTBR-tau243 is already known to be elevated in Alzheimer's disease. It is also raised in other brain diseases that share the same kind of toxic protein buildup, CTE among them. The researchers tested blood from 11 people whose CTE had been confirmed at autopsy. Levels of the fragment were higher than in healthy people, and they rose in step with the severity of the brain disease.
The limits are plain. The test could separate people with advanced CTE from healthy people with high accuracy, but it could not reliably pick up early-stage CTE. The sample was small, and the test has not yet been validated for diagnosing CTE. If large studies confirm the results, the authors say, clinicians could use a blood test to monitor people at risk and could run trials of drugs that might help the condition.
"We are potentially opening a new door for diagnosing and treating CTE in living patients," said Kanta Horie, co-senior author of the study. His co-author, the neuroscientist Chihiro Sato, was careful about how the marker would be used. "Our study shows that an Alzheimer's disease biomarker can be applied to other tauopathies, including CTE," she said. "This is not going to be a standalone biomarker. But if someone has a history of repeated head injury, tests negative for Alzheimer's and this biomarker comes up, it might be CTE."
The work lands amid continuing concern in science and sport. In one recent study of nearly 400 NFL players whose brains were donated after death, 93.5% showed evidence of CTE. More than 350 NFL players have been diagnosed with the disease posthumously, including Mike Webster, a hall of fame center; Junior Seau, whose 20-year career included two Super Bowl appearances; and Frank Gifford, a former MVP and prominent broadcaster.
In rugby, legal action continues from a number of living former union and league players who have been diagnosed with Traumatic Encephalopathy Syndrome, including the England World Cup winner Steve Thompson. The boxer Ricky Hatton received a diagnosis of mild CTE after his death. Earlier this year the Professional Footballers' Association recommended, as part of a CTE prevention protocol, that professionals head the ball no more than 10 times a week in training and that children under 12 not head it at all.
What to watch for now is validation: larger studies that test whether eMTBR-tau243 holds up for CTE, and whether it can ever reach the early stages where the current version falls short.
Citations marquantes
We are potentially opening a new door for diagnosing and treating CTE in living patients.— Kanta Horie, co-senior author, JAMA Neurology study
This is not going to be a standalone biomarker.— Chihiro Sato, neuroscientist and co-author