Kyle Wagner has an interesting piece on Deadspin looking into the latest frontiers in football and CTE, including the possibility of a live diagnosis:
While we don't have a cure for CTE's closest analogs, having that starting point makes a big difference. If we can see how the disease unfolds, we have a chance of stopping it. Thus: Gary Small's UCLA research into scanning living subjects. It's funded by BIRI, which was founded by Omalu, Bailes, and Robert Fitzsimmons. At the center of the study is a patented radioactive biomarker that Small co-invented for diagnosing Alzheimer's disease.The marker attaches itself to both tau protein tangles and amyloid plaques, the two elements necessary to diagnose Alzheimer's. There are other markers that attach to plaques, but this specific marker, [18F]FDDNP, is the only one known to lock onto tau. In the absolute simplest terms, this is the only known substance in the world that can make CTE show up on a scan in living patients.PET imaging tech is half a century old, and though FDDNP is relatively new, it's still been around for years. So it's strange to think about the marker being on the cutting edge of a fairly recently discovered brain disease. If the marker can find and pinpoint CTE, why hadn't anyone tried it before now? And for that matter, why isn't it already in use?
Think of it this way: In a collision, the brain is basically driving without a seatbelt or an airbag. While better helmets and the banning of helmet-to-helmet detonations might help keep your skull intact, they would do nothing to stop the brain from smashing into the windshield in even minor collisions. So how do you stop the brain from taking a beating on every routine block, tackle, and other impact--the real killers? Bailes's answer to this brain slosh amounts to stuffing the whole car full of packing peanuts.His newest research takes groups of rats and puts a small, circular device around their necks, compressing their internal jugular veins. That increases the volume of blood in the skull, which creates added pressure on the brain, locking it in place. In theory, that should keep the brain's movement inside the skull more in line with the skull's own movement, allowing all the new space-age helmets to do their jobs.So far, Bailes's team has seen a 30 percent increase in cranial pressure, and, after concussing the rats and examining the resulting computer models, an 80 percent drop in the precursors to amyloid protein. "This was only a proof-of-concept pilot study, and it hasn't been proven in humans, but we think the theory is sound," he said. "If it moves forward, we're going to expand to a broader group of patients, and we hope to do that sooner rather than later."
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