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Four ex-NFL players unite to launch largest ever CTE study

Four former NFL players have joined the largest study to date into the football-linked brain disease CTE that could lead to a test for athletes during their lifetime.

The program, launched today, is the passion project of another former player Jim Joyce, who played for the Denver Broncos before founding biotech firm Exosome Sciences to investigate the diseases that afflict thousands of players in later life.

In a world-first, researchers will monitor the biggest ever cohort of living current and former players – around 200 – for years to identify biomarkers associated with chronic traumatic encephalopathy (CTE), the disease linked to hard head-hits which causes dementia, aggression and suicidal thoughts.

Among others, it will include 53-year-old Solomon Wilcots, former Cincinnati Bengal and NFL broadcaster, 57-year-old Steve Jordan, former Minnesota Viking, and 44-year-old Jamir Miller, former Arizona Cardinal and Cleveland Brown – as well as Joyce himself.

While the players will have no idea of the findings or results, the ambitious investigation could lead scientists to a test for CTE during life.

Currently, the neurodegenerative condition can only be diagnosed in an autopsy.

Former Bengals player and current sports anchor Soloman Wilcots, 53, has joined the largest ever cohort study on living players to assess biomarkers to find a cure for the disease CTE

Steve Jordan

Jamir Miller

Tight end Steve Jordan, now 53, and linebacker Jamir Miller, now 44, (pictured left and right, respectively, during their times at the Minnesota Vikings and the Browns) have also joined

The announcement on Thursday morning comes just days after ex-con former player OJ Simpson, 70, said he fears he has CTE as he is forgetting names and numbers and people, but will never know for certain since there is no test. 

He is hardly the only player to speak out. 

Simpson’s words followed a slew of players’ agonizing accounts of mental decline, not to mention the scores of players’ deaths from suicide.

Brain degradation from repeated head hits is not a newly-discovered phenomenon – it has been recorded in boxers since the early 1900s. 

But in the last few years, we have seen an unprecedented surge in awareness as the 1960s generation – the first who used helmets, and therefore could hit their heads harder – reach their twilight years, and share harrowing accounts of their symptoms. 

That is one of the biggest wake-up calls for former players, Miller said at the launch for the Exosome study on Thursday.

‘I’ve lost friends,’ he said bleakly.

‘That’s it, I’ve lost friends – that, really, could still be contributing to society in a positive way. But [they’re gone] because of a debilitating condition that can’t even be diagnosed until you’re dead.

‘Until we can figure that bit out, the mystery, we can’t figure out a treatment plan.’

Miller, who is also the president of the NFL retired players association in Phoenix, said on Thursday that he hopes to involve as many living players as possible. 

‘I really understand that being at the age I am now, I’m understanding my mortality.

‘There’s this mystery that surrounds CTE. That’s why I’m here to support to give them all the resources to the chapter in Phoenix.’ 

Steve Jordan, 57, a former Minnesota Viking player, concurred.

‘It’s simply personal,’ he said. ‘As former athletes we have a lot of friends that have gone down as a result of CTE.’

But, he added, ‘it affects a lot of people, not just athletes’.

‘Even a subset of youth sports come into play,’ he said, ‘and a lot of people don’t talk about the military, they’re subject to head trauma.

‘Information will be the key to subjects like this to bring on some treatments and provide some solutions.’  

The Exosome study, running ‘in parallel’ with Boston University’s federally-funded CTE research program, is an attempt to confirm their belief: that they have found a biomarker which could be isolated in a blood sample to diagnose CTE.

The first sign of this possible biomarker, dubbed TauSome, was described in a scientific paper published in a journal in 2015. 

Now, Exosome needs to reach full enrollment – aiming for 200 players over the age of 20 with years of experience playing the game – to assess whether this biomarker can work in practice to match players’ symptoms to brain changes.  

‘Until CTE can be diagnosed in the living it is very unlikely that a treatment could emerge,’ Joyce said on Thursday.

The study is one of a handful of highly-anticipated research programs all racing towards the pot of gold at the end of the rainbow.

The neuroscience and pharmaceutical industry is well aware that a during-life test, and even preventative medicines, would be as lucrative (and beneficial for people) as an Alzheimer’s cure.

Money aside, it has immense support from players and fans – and as the wait for a cure or test drags on, the rate of kids taking up tackle football is steadily declining.   

This support has swelled as players share their emotional accounts – largely in a bid to tear down the NFL’s roadblocks to getting compensation.


by Alex Raskin, Sports News Editor 

A class action settlement brought against the league by over 20,000 retired players affected by concussions resulted in the NFL being forced to dole out $1 billion of payments over the next 65 years. On average, each player will receive about $190,000, while individuals can receive up to $5 million depending on the degree of the injuries sustained as well as the number of years they played in the NFL.

But while the settlement awards up to $4 million for past CTE deaths, it can’t do anything for players living with CTE because the disease cannot be diagnosed in the living. 

That’s a problem because players can be suffering from CTE without a long history of concussions.  

Deceased Patriots tight end Aaron Hernandez, for instance, had only one official concussion during his time in the NFL but was still posthumously diagnosed with a severe case of the CTE by Boston University’s CTE Center.

The situation is particularly problematic for players such as offensive lineman, who experience thousands of sub-concussive hits per season without ever officially registering a concussion.

A year ago, the U.S. Supreme Court denied challenges to the settlement, which means for now, the families of players who suffered from CTE may have trouble collecting any payments unless there are documented cases of concussions.

That doesn’t mean CTE will never be recognized as part of the settlement, but until it can be scientifically diagnosed in the living, the league won’t be able to compensate those enduring the disease on a day-to-day basis. 

Mark Gastineau, 64, wept live on the radio last week, telling host Pete McCarthy football had ruined his life. Diagnosed with Alzheimer’s, dementia, Parkinson’s and probable CTE, the former New York Jets star said he can no longer do simple tasks like tending the yard, and relies on his wife to be his primary carer.

Last month, Emily Kelly, wife of former New Orleans Saints player Rob Kelly, 43, wrote a searing op-ed for the New York Times, describing her husband as a paranoid, aggressive ‘ghost’ who regularly muses about suicide, forgets to eat for days on end, and lashes out uncontrollably. 

Larry Johnson, 38, who played for the Kansas City Chiefs, said he is convinced he has CTE after ‘demons in his head’ almost drove him to ‘jump off a roof’. 

Nick Buoniconti, 77, who played for the Dolphins, also wept as he pledged his brain to CTE research, having been diagnosed with dementia, likely CTE, and atrophy in his right frontal cortex which affects his balance. 

Aaron Hernandez, Junior Seau, and Dave Duerson, among others, were diagnosed with CTE after taking their own lives following illustrious careers in football. 

More than 1,800 former NFL players, boxers, and military veterans have pledged to donate their brains to the Concussion Legacy Foundation for CTE research.

Boston University has made huge headway in investigating chronic traumatic encephalopathy (or, CTE), the Alzheimer’s-like disease which has been linked to repeated blows to the head from contact sports.

Researchers are still unclear on how CTE affects behavior, but a growing swell of studies is offering some answers.

  • CTE sufferers have clumps of tau protein built up in the frontal lobe, which controls emotional expression and judgment (similar to dementia)
  • This interrupts normal functioning and blood flow in the brain, disrupting and killing nerve cells
  • By stage 3 – i.e. Aaron Hernandez’s stage – the tau deposits expand from the frontal lobe (at the top) to the temporal lobe (on the sides). This affects the amygdala and the hippocampus, which controls emotion and memory

One of Boston University’s papers published in 2017 found those who start playing football from before the age of 12 – as most professional players do – have a much higher risk of mood, behavioral and neurological problems in later life compared to those who start later. They attributed this to the damage of repeated hits to the head at such a critical time of brain development.

Another showed 110 of the 111 former players brains they had in their lab, donated from families after death, had signs of CTE, showing that it’s not a trivial number of people that get the crippling disease.

Perhaps most importantly, last month Boston published a groundbreaking study to demolish the obsession with concussions.

Concussions, they found, are the red herring: it is not a ‘big hit’ in football that causes CTE or makes it more likely. Rather, it is the experience of repeated subconcussive hits over time that increases the likelihood of brain disease. In a nutshell: any tackle in an NFL game – or even practice – increases the risk of a player transforming into the ‘ghost’ of a human, according to Dr Stern.

This year, the team has published a slew of research papers showing links between football and brain injury.

While there is still no way to diagnose the disease during life, the evidence bridging the gap between head hits and neurodegenerative diseases is strengthening at an unprecedented rate.

‘I don’t know of any other area of scientific investigation that has had such a large and pure impact on awareness in lay culture and attention within the scientific community,’ Dr Robert Stern, head of Boston’s CTE research unit, told Daily Mail Online this week.

‘This has been a landmark year for media coverage and cultural awareness of CTE and long-term consequences of playing football.

‘We still have a tremendous amount of work ahead of us to be able to answer some very important questions about CTE, but we should have a test to diagnose in life within the next five to 10 years – and that’s being conservative.’ 

Aaron Hernandez had the most severe CTE case ever seen: Scientists found 27-year-old’s brain tissue showed extreme damage to memory and impulse control

by Mia De Graaf, Health Editor

The neuroscientist who analyzed Aaron Hernandez’s brain confirmed that he suffered the worst case ever seen in someone so young, with severe damage to regions that affect memory, impulse control and behavior.

The 27-year-old former New England Patriots player killed himself in April 2017 while serving life in prison for murder.

In September, Dr Ann McKee of the CTE Center at Boston University posthumously diagnosed Hernandez with chronic traumatic encephalopathy, a football-linked disease that causes dementia and aggression.

Aaron Hernandez was a star tight end for the New England Patriots on a $41 million contract when he was arrested for double murder. in June 2013. Four years later, while serving life in prison, he took his own life. He was posthumously diagnosed with the worst case of CTE ever seen in a football player

Aaron Hernandez was a star tight end for the New England Patriots on a $41 million contract when he was arrested for double murder. in June 2013. Four years later, while serving life in prison, he took his own life. He was posthumously diagnosed with the worst case of CTE ever seen in a football player

She formally presented her findings a month later, and confirmed that she had never encountered such extreme degradation in a young brain, pointing out areas of severe tissue damage and microbleeds likely caused by blows to the head.

They also found a variant of the APOE gene, which has been linked to increased risk of Alzheimer’s, but the scientists emphasized that no gene could inflict the same damage as years of heavy impact from tackling.  

Dr McKee says she could not say for certain that Hernandez’s criminal and suicidal acts were a result of his severe case of CTE, nor whether other 27-year-old players could plausibly have the same pathology. But she says Hernandez suffered substantial damage to several important regions, including the frontal lobe.

‘In this age group, he’s clearly at the severe end of the spectrum,’ McKee said. 

‘There is a concern that we’re seeing accelerated disease in young athletes. Whether or not that’s because they’re playing more aggressively or if they’re starting at younger ages, we don’t know. But we are seeing ravages of this disease, in this specific example, of a young person.’ 

Hernandez was diagnosed with stage three out of four, with four being the most severe.

This picture shows a scan of Hernandez's brain compared to that of a normal 27-year-old. It shows severe decay in the center of his brain from CTE

This picture shows a scan of Hernandez’s brain compared to that of a normal 27-year-old. It shows severe decay in the center of his brain from CTE

His brain scans reveal huge clumps of tau protein in Hernandez’s frontal lobes, and in the nerve cells around small blood vessels, a unique feature of CTE.

These proteins, also seen in dementia, disrupts the normal functioning of the brain, triggering aggressiveness, explosiveness, impulsivity, depression, memory loss and other cognitive changes. 

Dr McKee cautioned that she has not received many brains of players so young who played to such a high level as Aaron Hernandez, who started playing before the age of eight and was regarded as one of the NFL’s top tight ends.

The tests showed Hernandez had early brain atrophy and large perforations in the septum pellucidum, a central membrane which is essential to control behavior.

Hernandez’s brain scans revealed he had a variant of the APOE gene, which has been linked to neurodegenerative diseases like Alzheimer’s, a similar disease to CTE. However, CTE uniquely affects certain nerve cells which Alzheimer’s appears not to. 

Hernandez was indicted in August 2013 (pictured). He was convicted of first-degree murder, and sentenced to life in prison in April 2015

Hernandez was indicted in August 2013 (pictured). He was convicted of first-degree murder, and sentenced to life in prison in April 2015

The disgraced star had a $41 million NFL contract when he was arrested at his home in June 2013 and charged with the murder of a semi-pro football player Odin Lloyd.

Lloyd was the boyfriend of Hernandez’s fiancee’s sister. He was found dead in an industrial park on June 17, 2013, riddled with bullets. Surveillance footage showed Hernandez at the scene an hour before, then arriving at home minutes after gunshots were fired. 

In April 2015, Hernandez was convicted of first-degree murder, and sentenced to life in prison.

While in prison, Hernandez was charged with another killing – a double murder committed by a drive-by shooting. But in April 2017, he was acquitted of both charges.

The next day, he took his own life. 

His family has since filed a lawsuit against the NFL and the Patriots on behalf of Hernandez’s four-year-old daughter Avielle, claiming the club and the league knew about the connections between football and CTE long before Hernandez was drafted.