Earlier this summer, Dr. Charbel Moussa, director of the Georgetown University Laboratory for Dementia and Parkinsonism, presented a possible treatment for dementia and Parkinson’s at the Alzheimer’s Association International Conference in London.
In previous research, Moussa had discovered a way to treat one of the underlying physical causes of dementia and Alzheimer’s, as well as a host of other neurodegenerative diseases. Many such neurological conditions are marked by an abnormal amount of certain proteins (specifically, tau and amyloid), and Moussa had found a way to clear the brain of this “toxic buildup” — and in turn, reduce brain inflammation and improve cognitive performance.
Immediately, some people began asking him about whether the treatment could also be applied to chronic traumatic encephalopathy, or CTE, the brain disease that’s dominated headlines and beleaguered the sport of football for the past decade. An accumulation of tau proteins in the brain is the signature characteristic of CTE, and Moussa’s research seemed a natural fit for the infamous disease.
The only problem? Despite the NFL and other football organizations saying they’re taking the threat of CTE seriously, no one will fund a CTE-specific version of Moussa’s work.
“We’ve had several attempts to start clinical trials with CTE,” says Moussa. “There’s a lot of interest, but unfortunately it comes from individuals, and not institutions that want to finance a trial.”
CTE first burst into the mainstream 15 years ago, when forensic pathologist Bennet Omalu discovered the first case in a former NFL player when he conducted an autopsy on former Pittsburgh Steelers center Mike Webster. More than 100 more cases have been discovered since then.
Moussa’s proposed treatment involves repurposing cancer treatments for use in the brain. More specifically, last year, Moussa released the results of a phase I clinical trial that showed how nilotinib, an FDA-approved leukemia drug, and other medications significantly reduced the amount of toxic proteins in the brain. The drugs activate a natural cleaning process called autophagy, where the brain rids itself of excess proteins. “The brain turns on its garbage disposal and starts to degrade all the toxic buildup of the tau protein,” Moussa explains.
Tau buildup often causes the brains of CTE patients to look withered and ravaged with plaque. Clearing it wouldn’t necessarily allow the brain to regain any brain matter that had been lost — “brain regeneration is nonexistent,” Moussa says — but it would likely prevent further damage. “These drugs would be good candidates for CTE, and they particularly would be beneficial to prevent the long-term toxicity of any brain injury,” Moussa says.
Moussa met with the NFL Players Association in early 2016 about having them fund a study, but the NFLPA declined, according to Moussa. It was only interested in backing CTE-related research that could be conducted on animals, and Moussa was proposing a human trial, he says. (Neither the NFL or NFLPA returned requests for comment.) “To have a clear insight into whether something works or not, you have to move to human trials,” Moussa says. “We might not be able to get the results we hope for, but if we test this drug in a clinical trial, we’ll know for sure.”
Moussa says he’s open to working with researchers at Boston University and/or UCLA, both of which are the forefront of sports concussion research, but the reality is that research universities tend to prioritize their own initiatives over collaboration. He even approached the Defense Department about funding — brain injuries are common on the battlefield — but they, too, passed. “They don’t want to look like they’re using soldiers as guinea pigs for a medical experiment,” Moussa says.
The fact that Moussa can’t secure funding for a simple exploratory trial is baffling considering all the attention surrounding CTE, and the fact that the drugs he’s proposing have already shown promising results in treating Parkinson’s and dementia.
The cost is fairly negligible as well. Moussa estimates that a six-month trial would cost $1 million, a pittance relative to the $13 billion in revenue the NFL made last year, and disgraceful when you consider the NFL didn’t fulfill its promise to donate $30 million to the National Institutes of Health for concussion research.
Not to mention, there’s a lot of money to be made here. There’s currently no treatment for CTE, and anyone at risk for the disease is likely to pounce at the opportunity to take such a treatment. The NFL should be just as eager to provide it (if, of course, it passes the trial phase) — for no other reason than to help put the ongoing CTE PR crisis behind it. And the potential applications for Moussa’s research extend far beyond just CTE, which, despite its notoriety, afflicts only a small proportion of the population.
“The promise and the hope of these drugs far outweighs the cost,” Moussa says. “One million dollars is a lot less than the amount of care you’d need for someone suffering from CTE or a random brain injury over the course of 30 years.”
