Here's a question nobody wants to ask at a rugby reunion: what's happening inside the brains of people who spent years getting tackled for a living? A study in Journal of Neurology, Neurosurgery & Psychiatry went looking for answers in the blood of former elite rugby players, and what they found isn't exactly reassuring. Even in midlife, years before any dementia symptoms showed up, these athletes already had protein signatures that look a lot like early Alzheimer's and CTE.
The good news? We might be able to catch this early. The complicated news? We're still figuring out what to do about it.
The Sport That Keeps on Giving (In the Worst Way)
Rugby is a beautiful, brutal sport. It's also one where your head takes a beating. Unlike concussions that knock you out cold and send you to medical tents, most of the damage comes from repeated subconcussive impacts. The kind you barely notice. The kind you walk off. The kind that, apparently, your brain is quietly keeping track of.
Former contact sports athletes have higher rates of neurodegenerative dementia. This isn't speculation anymore; it's been documented in American football players, soccer players, and yes, rugby players. The pattern is consistent enough that we stopped asking "if" and started asking "how bad" and "how early."
CTE (chronic traumatic encephalopathy) gets a lot of attention because it's dramatic, but these players are also at elevated risk for regular Alzheimer's disease. Both conditions involve abnormal protein accumulation in the brain, just with different geographic signatures and different timeframes.
What Blood Proteins Tell Us About Hidden Brain Changes
Here's where the science gets clever. You can't exactly biopsy someone's brain to see if they're developing problems. But proteins from the brain do leak into the bloodstream, and with sensitive enough tools, you can detect them. It's like reading smoke signals from a fire you can't directly see.
The researchers used ultrasensitive immunoassays to measure specific proteins in blood samples from former elite rugby players. These weren't elderly retirees showing obvious symptoms. These were midlife adults, seemingly healthy, living their post-rugby lives without obvious cognitive problems.
What showed up in their blood told a different story.
The Amyloid-Tau Double Punch
If you've heard anything about Alzheimer's disease, you've probably heard about plaques and tangles. Plaques are clumps of amyloid protein that accumulate between brain cells. Tangles are twisted fibers of tau protein that build up inside cells. Together, they're the molecular signatures of a brain in trouble.
The rugby players showed altered levels of multiple proteins involved in both amyloid and tau processing. Not just one marker slightly off, but a pattern of changes suggesting their brains were already handling these proteins differently than control subjects.
This is worth pausing on. These are people in their 40s and 50s, decades away from typical Alzheimer's onset, already showing blood-based evidence that something is brewing. Their brains are processing the same proteins that go wrong in dementia, and they're doing it abnormally.
CTE has its own protein signature, with tau accumulation in characteristic patterns around small blood vessels. The proteomic changes in these rugby players showed overlap with both CTE and AD pathways. Their brains might be developing both types of pathology, or developing something that shares features with each.
The Promise and Problem of Early Detection
So we can potentially detect brain pathology from a blood draw before symptoms appear. That sounds great until you ask the obvious follow-up: then what?
Right now, there's no proven way to stop or reverse amyloid and tau accumulation once it starts. The handful of anti-amyloid drugs that have been approved have modest effects and significant side effects. We're still figuring out whether removing amyloid actually helps, or whether it's too late by the time pathology is detectable.
But here's the counterargument: knowing is still better than not knowing. Former athletes who learn they have elevated risk might be more motivated to optimize the factors we do know matter. Exercise (the right kind, without head impacts). Sleep quality. Cardiovascular health. Cognitive engagement. Social connection. These won't reverse protein accumulation, but they might build cognitive reserve that helps the brain compensate.
Early detection also enables monitoring. If you know someone is at elevated risk, you can track them over time, catch actual cognitive decline earlier, and potentially intervene when treatments do become available.
What This Means for Current and Former Athletes
If you played contact sports at any level, this research lands differently than if you're just a casual reader. The question becomes personal: is this happening in my brain?
The honest answer is we don't know for sure. Elite athletes took more impacts over longer careers, so they represent an upper bound of exposure. Weekend warriors with less cumulative head trauma might have lower risk. But we don't have good data on where the threshold is, or even if there is a clean threshold versus a dose-response curve where every hit adds up.
The practical implications are still being worked out. Should former contact sports athletes get routine blood protein screening? Who pays for it? What do we tell people when their numbers are concerning? The science is outpacing the healthcare infrastructure and the policy frameworks.
For now, what we can say is this: the link between head impacts and later brain pathology is real, detectable earlier than we thought, and probably worth taking seriously if you've spent significant time in contact sports. The conversation about whether the trade was worth it is one each person has to have with themselves.
Reference: Bhattacharyya S, et al. (2025). Midlife plasma proteomic profiles indicate altered amyloid and tau processing in former elite rugby players. Journal of Neurology, Neurosurgery & Psychiatry. doi: 10.1136/jnnp-2025-335123 | PMID: 41047224
Disclaimer: The image accompanying this article is for illustrative purposes only and does not depict actual experimental results, data, or biological mechanisms.