A military brain bank found no definitive CTE among 163 donors
A decade-on review of chronic traumatic encephalopathy research reports that 5 of 70 veteran donors had features of the pathology and none met the full definition. A small UK rugby study looks elsewhere.
Chronic traumatic encephalopathy is discussed publicly as a settled diagnosis with a known prevalence among people exposed to repeated head impacts. Two papers published within days of each other this month illustrate how far the underlying science is from that description — one by counting the pathology in a brain repository and finding very little of it, the other by looking for a blood signal in living former athletes.
The decade-on review
The first is a commentary in Military Medicine revisiting priorities set at a 2015 International State-of-the-Science Meeting held by the Department of Defense Blast Injury Research Program Coordinating Office [s1]. That meeting identified two top priorities: more research on CTE neuropathologic change, and more research on clinical diagnostic criteria [s1]. The commentary reviews what the intervening decade produced and adds new data of its own [s1].
The new data come from the Lieber Institute for Brain Development brain repository. Donors were 163 men with a mean age of 66 at death, range 50 to 96 [s1]. Seventy of them — 42.9% — had served in the military, and 15 (9.2%) reportedly experienced combat [s1]. Tissue was screened for definitive CTE neuropathologic change or for "features" of it [s1].
No case had definitive CTE neuropathologic change [s1]. Features of it appeared in 4 of 93 civilian donors (4.3%) and 5 of 70 veteran donors (7.1%) [s1].
The authors' reading is that it is unclear how common CTE neuropathologic change is in military veterans, and that it is possible it is uncommon [s1]. They also state that there are no validated clinical diagnostic criteria for CTE, and that recent studies have shown CTE neuropathologic change is not associated with depression, suicidality, anxiety, irritability, impulsivity, explosivity, verbal violence, physical violence or substance abuse [s1].
That last list matters, because those symptoms are the ones most often attached to CTE in public discussion.
Why this differs from the numbers people know
The widely cited high prevalence figures for CTE come from brain banks assembled through donation by families who suspected the condition — a recruitment route that selects for cases. A repository not built around suspected CTE gives a different denominator, and the difference between the two is not a contradiction so much as a different question being answered.
The Lieber repository sample is also not a random sample of anything. It is 163 men, disproportionately military [s1], whose brains were donated for reasons the commentary does not enumerate. A finding of zero definitive cases in that group establishes that definitive CTE is not routine in this repository; it does not establish a population rate.
Looking in the living
Because CTE can currently only be confirmed after death, the parallel research effort is to find something measurable in living people. A study published three days later in the International Journal of Molecular Sciences took the biomarker route in retired rugby players [s2].
The researchers compared serum levels of 24-hydroxycholesterol, 25-hydroxycholesterol, 27-hydroxycholesterol, total triglycerides and ceramide between 26 retired rugby players with a history of repeated concussions and 19 non-contact-sport controls, alongside cognitive scores [s2]. Quantification was by ELISA [s2].
The concussed group had significantly lower serum 24-hydroxycholesterol and significantly higher 27-hydroxycholesterol, triglycerides and ceramide than controls; 25-hydroxycholesterol did not differ [s2]. The authors report that repeated concussion was associated with reductions in cognitive performance and persistent alterations in serum lipid profiles, and propose the lipid changes as a possible foundation for future work on monitoring neurological health in at-risk populations [s2].
24-hydroxycholesterol is of interest here because it is produced almost exclusively in the brain and crosses into circulation, which makes it one of the few peripheral markers with a plausible central origin.
The limits, stated plainly
Twenty-six players and nineteen controls is a small study, and it is cross-sectional: it compares two groups at one point in time and cannot establish that concussion caused the lipid differences [s2]. Retired contact-sport athletes differ from non-contact controls in more than head impact exposure — body composition, training history, current activity, and diet among them, all of which affect triglycerides and ceramide. The study does not report that these were matched or adjusted for.
Nor does it connect the lipid signal to CTE. The pathology defining CTE is a tau deposit pattern; a serum lipid difference is not evidence of that pathology, and the paper frames its findings as a foundation for future studies rather than a diagnostic test [s2].
Reading the two together
They point at the same gap from opposite ends. The Military Medicine commentary says there are no validated clinical diagnostic criteria for CTE and that the pathology may be less common than assumed, at least in one repository [s1]. The rugby study is an early attempt to find something measurable in people who are still alive, and lands on a plausible but non-specific signal in a small sample [s2].
Neither paper says repeated head impacts are harmless. The rugby study reports reduced cognitive performance in the concussed group [s2], and the broader literature on the consequences of repetitive head impact is not in question here. What both papers narrow is a more specific claim: that CTE is a well-characterised, commonly occurring, clinically diagnosable condition with an established symptom profile. On current evidence, three parts of that sentence do not hold.
What to watch
The commentary's framing implies the useful next step is validated clinical diagnostic criteria, which do not exist [s1]. On the biomarker side, what would move the rugby finding from interesting to useful is a larger, matched cohort with longitudinal sampling and, eventually, correlation against neuropathology at autopsy.
Sources
- Chronic Traumatic Encephalopathy Neuropathologic Change in Military Veterans — Military Medicine, 2025-11-10
- Concussion-Related Cognitive and Lipid Changes in Retired UK Rugby Players Study — International Journal of Molecular Sciences, 2025-11-13
Sources
- Chronic Traumatic Encephalopathy Neuropathologic Change in Military Veterans — Military Medicine , November 10, 2025
- Concussion-Related Cognitive and Lipid Changes in Retired UK Rugby Players Study — International Journal of Molecular Sciences , November 13, 2025
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