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Leading the fight against a formidable foe

Dr Charles Bernick is leading the largest study to date into punch drunk syndrome among professional athletes. The findings could help to identify the “breaking point” for brain injuries, he tells Sarah Sinclair.



On a Saturday night in February 2018, 31-year- old British boxer Scott Westgarth spoke of his love of the sport as he emerged triumphant from his match against Dec Spelman in Doncaster, England.

Hours later he collapsed in his locker room and was rushed to hospital, where he tragically died of head injuries sustained during the fight.

Then in July this year came two more boxing fatalities within a few days of each other. Both the Russian boxer Maxim Dadashev, 28, and 23-year-old Argentinian fighter Hugo Alfredo Santillan died from brain injuries, prompting fresh calls for drastic changes in the sport.

Boxers know they take a risk every time they enter the ring. Success is measured by the number of blows to the head delivered to your opponent, and has therefore long been controversial among campaigners.

Brain injury charity Headway has even called for it to be banned on several occasions. But while we often hear about what can go wrong inside the ring, boxing has a hidden danger less talked about.

American pathologist Dr Harrison Martland first described a group of boxers as being “punch drunk” in 1928.

His research paper gave a name to the phenomenon of boxers with a history of repetitive head trauma developing neurological symptoms.

Today punch drunk syndrome is better known as Chronic Traumatic Encephalopathy (CTE), the degenerative brain disease increasingly linked with rugby, football and injuries sustained in military service.

CTE, currently only diagnosed after death through brain tissue analysis, has been confirmed in more than 50 former boxers, according to the Concussion Legacy Foundation in America, using data from the VA-BU-CLF Brain Bank in Boston.

“To put it simply, the more head impacts somebody gets, the greater the risk,” says neurologist Dr Charles Bernick, from his office at the Lou Ruvo Centre for Brain Health, in the self-proclaimed fight capital of the world, Las Vegas.

“It’s just that boxing is probably the sport that gets the largest number of head impacts, because that’s the whole goal.”

In 2011 Bernick and fellow researchers at the Ruvo Centre, which specialises in research and care of neurodegenerative diseases, launched the Professional Athletes Brain Health Study (PABHS).

It is now the largest longitudinal research project into the effects of repetitive impacts to the brain in a group of professional combatants.

The study currently has over 800 participants, at various stages in their careers; from active fighters at different levels to retired athletes of varying lengths of time – and others who are transitioning between the two.

“CTE is a neurodegenerative disease, it’s in the same category as other disorders such as Alzheimer’s and Parkinson’s, but although we’ve known about it for almost 100 years, nobody really understood it.”

Symptoms of CTE don’t generally begin to appear until years after the head impacts.

So while a boxer may seem to have walked away from a fight unscathed, the signs of long-term brain damage could show up in later life.

Former British Gold Olympian boxer Audley Harrison has spoken recently about the long-term impact his career has had, as he battles permanent brain damage, sight and balance problems and behavioural issues, such as mood swings.

Early symptoms affect the individual’s mood and behaviour, but as the disease progresses, some may experience memory loss, confusion, impaired judgment, and eventually progressive dementia.

From two experts at Boston University, Dr Ann McKee and Dr Robert Stern, we know that CTE can take two forms.

Some with CTE initially present with behavioural symptoms, usually in their late 20s or 30s, while others first show signs of cognitive problems, typically beginning in their 40s and 50s. What we don’t know is why it affects some people and not others.

“We thought this was a condition that we needed to learn more about, and being in Las Vegas, we had the means to do it,” says Bernick.

With his team, he set out to find out how CTE evolves, what the risk factors are and why only some boxers go on to develop the disease.

“We started working with key players, with the Nevada Athletic Commission (NAC) and some of the main organisations and top boxing promoters, to begin recruiting fighters, alongside a controlled group of non-fighters.

“We’ve been following these people on a yearly basis over that time, to try to really understand what happens.”

The open-ended study was set to last for at least 10 years, but as the decade draws to a close it looks likely to continue for as long as the funding is in place. Eight years in, it has made some stand-out findings.

While symptoms may not show up for many years after an athlete has left the ring, according to the research, in some cases, changes in certain areas of the brain can be detected by MRI methods within just a year of being exposed to repetitive head injuries.

These changes correlate with a decline in performance on tests of cognitive function, such as memory and thinking tasks.

The effects also differed between active and former fighters, with some evidence to suggest the disease actually progresses more quickly once a boxer retires.

And changes were also influenced by an individual’s genetic make-up, in older, former athletes.

Bernick says: “In some individuals you can track change over time, in certain areas of the brain, and it seemed to differ between active and retired fighters. Once they retire, there’s a subset of people that have this progressive process which may affect different areas of the brain. This is really interesting stuff as we try to develop ways to identify who might be at risk of CTE.”

The study has also discovered blood markers – certain proteins released from injured brain fibres which leak out of the brain and can be measured in the blood.

They could be used to identify brain injury and follow recovery, and changes in MRI imaging that may be able to track an injury.

It is hoped this will lead them to identifying the “breaking point” – the point at which repeated head trauma begins to cause cognitive problems for a boxer, and could lead to serious brain conditions such as CTE.

Researchers are also exploring how changes in behaviour correlate with brain imaging changes. Behavioural issues are common in the early stages of CTE, with symptoms including impulse control problems, aggression, paranoia and depression.

In April 2019, Bernick and co published a paper linking symptoms of depression in some athletes to structural brain changes associated with CTE; but the pathologist is eager to state it as “cause and effect”.

“Depression is complicated, because there’s the issue of what happens in the brain and the issue of other surrounding factors, such as family history, life circumstances, drug and alcohol use, which makes it difficult to tease out how much is really from the head impact.

“The prevalence of depression in our group was the same as the general population of men at that age, but in those who have depression there was a correlation with smaller regional volumes in certain areas of the brain.

“It suggests that there is a relationship between what’s changing in the brain and the manifestation of depression and other behavioural changes.”

There is also preliminary evidence to suggest that symptoms of depression could even appear before noticeable cognitive changes in someone with CTE.

Far from banning boxing, however, researchers hope that the findings will help to guide new practices to improve brain health in the sport and ultimately, make it safer.

“There is no question that there is great value in boxing. It’s an outlet, and there’s a clear societal benefit to these sports.

“It’s just a matter of how we make them safe.

“In the US, even though the main risk of fighting is to the brain, there is no requirement for any brain tests, except for an MRI scan. “Looking at the risk factors, whether it’s genetic, environmental or lifestyle, might help to protect an athlete as they play these sports.”

Few boxers have spoken publicly about CTE, perhaps for fear of giving the sport a bad name.

Yet, those in the industry have been right behind the study from the beginning, says Bernick, particularly representatives of the NAC, which provides the athletes for the study.

“The first goal of the NAC is to advocate and protect the safety of unarmed combatants,” says Dr Timothy Trainor, consulting physician to the NAC.

“When we partnered with the Ruvo Centre years ago, it was the vision of both the NAC and the Ruvo Centre to see if we could make meaningful progress in the diagnosis and treatment of CTE and brain injury. Anything we can do to promote the safety of an inherently risky sport is our first objective.

“The NAC has stressed the importance of this study to all of our licensed unarmed combatants, including boxers, mixed martial artists and kickboxers, and we are hoping the data gleaned from the study can better help us protect the athletes from harm, both short and long term.”

As a result of the study, the NAC is now looking into ways to actively protect its fighters, and identify potential problems sooner.

“We have learned that we need to focus more on functional studies as opposed to static anatomy tests like MRI/MRA,” says Trainor.

“Certainly, the study is pointing us in other directions that need further study. “One specific test that we have looked at extensively is the ‘C-3 Test’, a cognitive function test performed on an iPad.

“We have tried to implement this in our jurisdiction, however, the logistics of conducting such a test have proved insurmountable.

“We are continuing to try to find tests that will not be logistically prohibitive to the athletes.”

But, he adds: “Just the fact that the studies are being performed has raised the awareness of brain health to the fighters, trainers, and all involved in these sports.”

Things in the boxing ring are certainly changing. Fighters are reportedly sparring less and choosing their opponents more carefully.

In a 1973 study by British pathologist John Corsellis, the boxers participating were exposed to between 300 and 700 bouts over the course of their careers, in addition to sparring and other training.

Today a professional boxer would rarely see upwards of 50 fights before retirement.

But as far as Bernick is concerned, this in no way means athletes today don’t run a substantial risk of suffering a neurological hangover from their careers.

“What we’ve learned from 40 to 50 years ago may not be exactly what the risk is for modern day fighters,” he says.

“But we know that the more exposure you have to head trauma, the higher the risk of CTE.”

Thankfully, many in the boxing world appear to be waking up to dangers of the sport and taking research evidence on board.

Bernick would like to see such recognition in other sports too.

“If all sports took some responsibility for the long-term health of these athletes, not just when they are playing, I think it would be a real step forward for safety in sports.”

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Impact during TBI can have effects years later – study



Researchers from Imperial College London helped lead the study

The force exerted on the brain during traumatic injury is linked to damage years after the initial event, research has revealed.

Findings of the new study have been hailed as having the potential to predict the severity of brain injuries and help influence new approaches going forward, particularly in the field of sport.

TBI has a number of immediate impacts, including physical effects like unconsciousness and bleeding, alongside the ‘hidden’ symptoms of memory loss, mood and personality changes, which may take much longer to develop.

However, the link between the mechanical forces that act on the brain during TBI and the resulting long-term changes is poorly understood.

Now, researchers from Imperial College London have shown a clear link between the forces acting on the brain during TBI and its associated long-term changes.

The study – ‘From biomechanics to pathology: predicting axonal injury from patterns of strain after traumatic brain injury’, which is published in Brain – combined a computational model of brain injury with experimental studies on rat brains.

“The initial damage during a traumatic brain injury takes only milliseconds to occur, but it triggers many changes that result in ongoing effects which can be felt years later,” says Dr Mazdak Ghajari, from the Dyson School of Design Engineering.

“Understanding the link between the two is crucial for predicting who is at risk for long-term damage, and how protection may be better designed to prevent this damage.”

The findings have the potential to make positive impacts in protective equipment, such as in the design of helmets.

Professor David Sharp, from the Department of Brain Sciences, says: “We are also looking at how the type of impacts experienced by American football players affects whether they lose consciousness, and whether new helmet designs might protect soldiers from the effects of blast waves following explosions.

“These types of studies can also help explain whether repeated small impacts, such as heading the ball in football, could lead to similar long-term brain injury.”

Previously, the team had built a human computer model to predict the location of long-term brain damage following TBI, focusing on the ‘white matter’ of the brain, which contains nerve fibres called axons which play a large role in the brain networks that are altered in long-term brain damage.

Now, they have tested this modelling approach to see if it can accurately predict the pattern of white matter damage in rats given mild or moderate TBI.

They simulated the rats’ brains during injury, revealing the location and duration of mechanical forces linked to damage. Using a precise experimental model, this damage was induced in the rat brain and followed up after several weeks, which correlates to years of changes in a human brain.

They found that the effect of shear stresses on the white matter helped to predict the location of long-term damage. Shear stresses push two parts of the same object, in this case the brain, in different directions.

The intensity of the shear at different locations caused by different impacts, for example what angle they come from, predicts where the most severe white matter damage will occur. This could potentially help doctors predict the likely long-term effects in patients who have suffered a TBI.

“Different types of injuries will cause different kinds of shear. With this new model we can now more accurately predict which injuries will cause severe, long-term damage, and potentially avert it,” continues Dr Ghajari.

“For example, motorbike accidents involve a lot of rotational movement, which causes lots of shear. We are studying dozens of bike helmets to see which best protect against excess rotation.”

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Groundbreaking research into MS could enable development of new treatments



The research comes from the MS Society Edinburgh Centre for MS Research

The types of nerve cells which are lost through developing Multiple Sclerosis (MS) have been identified for the first time, in a breakthrough which could yield the development of new nerve-protecting treatments.

In a new study, researchers found that the inhibitory interneurons are lost in people who have MS.

Previously, it was only known that myelin, the protective coating around nerves, is damaged in MS – but pinpointing the selective loss of specific nerve cells has now been established.

The research, from the MS Society Edinburgh Centre for MS Research, could now lead to steps forward in the development of treatments to help protect the nerves most at risk.

Using brain tissue samples from the MS Society Tissue Bank, Professor Anna Williams and her team found a dramatic reduction in the number of inhibitory interneurons in tissue from people who had been living with MS, compared to people without the condition.

Another type of neuron – stimulating neurons – remained the same, even in people who had MS for decades.

Current treatments for MS target the immune system and reduce damage to the myelin, but by identifying how to replace lost myelin and protect nerves is the goal for researchers – and has been brought closer by this research.

“Our research has shown that a specific type of neuron, called an inhibitory interneuron, is damaged in people with MS,” says Professor Williams, who led the study.

“This is really important because, in the search for new treatments, it focuses our efforts on trying to stop the damage and death of these special cells.

“Our next step is to convert this knowledge into new treatments that protect nerves and prevent neurodegeneration – and ultimately disability – in people living with MS.”

The research team also generated a new mouse model of myelin damage, which showed the same selective loss of inhibitory neurons seen in humans – showing that myelin damage leads directly to nerve damage.

Researchers will now be able to test new treatments in the mice to see if they can prevent the inhibitory neurons from being damaged. This will help develop new treatments to protect nerves in MS.

Dr Lida Zoupi, who worked on this study, says: “In our mouse model, we show that demyelination directly leads to neurodegeneration, answering a long-standing debate between MS researchers in the process.

“By confirming this, we have a vital new insight into the mechanisms behind neurodegeneration, which could potentially be used as a model for the development of neuroprotective treatments.”

The research was hailed as a vital step in the ongoing efforts to understand MS and develop treatments as a result.

“We’ve made huge progress in finding treatments that target the immune system, but many people living with MS still don’t have access to effective treatments,” says Dr Emma Gray, assistant director of research at the MS Society.

“We believe this study represents a vital step in our mission to stop MS.

“Work like this, which is based at our Edinburgh Centre and used samples from the MS Society Tissue Bank, shows just how important charity funded research is to the overall research landscape, and we’re proud to have made it possible.”

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Landmark breakthrough in understanding Alzheimer’s



Brain cells vulnerable to Alzheimer’s Disease have been identified for the first time, in a breakthrough scientists hope could lead to targeted treatments to boost the brain’s resilience.

It has so far remained unknown in Alzheimer’s research why some brain cells succumb to the disease years before symptoms first appear, while others seem unaffected by the degeneration surrounding them until the disease’s final stages.

Now, in a groundbreaking study, the neurons that are among the first victims of the disease –  accumulating toxic ‘tangles’ and dying off earlier than neighbouring cells – have been identified for the first time.

“We know which neurons are first to die in other neurodegenerative diseases like Parkinson’s disease and ALS, but not Alzheimer’s,” says co-senior author Martin Kampmann, associate professor in the UCSF Institute for Neurodegenerative Diseases.

“If we understood why these neurons are so vulnerable, maybe we could identify interventions that could make them, and the brain as a whole, more resilient to the disease.”

Alzheimer’s researchers have long studied why certain cells are more prone to producing the toxic tangles of the protein known as tau, whose spread through the brain drives widespread cell death and resulting progressive memory loss, dementia, and other symptoms.

But researchers have not looked closely at whether all cells are equally vulnerable to the toxic effects of these protein accumulations.

“The belief in the field has been that once these trash proteins are there, it’s always ‘game over’ for the cell, but our lab has been finding that that is not the case,” said Lea Grinberg, senior co-author and associate professor in the UCSF Memory and Ageing Centre.

“Some cells end up with high levels of tau tangles well into the progression of the disease, but for some reason don’t die.

“It has become a pressing question for us to understand the specific factors that make some cells selectively vulnerable to Alzheimer’s pathology, while other cells appear able to resist it for years, if not decades.”

To identify selectively vulnerable neurons, the researchers studied brain tissue from people who had died at different stages of Alzheimer’s disease, obtained from the UCSF Neurodegenerative Disease Brain Bank and the Brazilian BioBank for Ageing Studies.

The São Paulo-based biobank collects tissue samples from a broad population of deceased individuals, including many without a neurological diagnosis whose brains nevertheless show signs of very early-stage neurodegenerative disease, which is otherwise very difficult to study in humans.

The team studied tissue from ten donor brains using a technique called single-nucleus RNA sequencing, which let them group neurons based on patterns of gene activity.

In a brain region called the entorhinal cortex, one of the first areas attacked by Alzheimer’s, the researchers identified a particular subset of neurons that began to disappear very early on in the disease.

Later in the course of the disease, the researchers found, a similar group of neurons were also first to die off when degeneration reached the brain’s superior frontal gyrus.

“These findings support the view that tau buildup is a critical driver of neurodegeneration, but we also know from other data from the that not every cell that builds up these aggregates is equally susceptible,” adds researcher Kun Leng.

“Our discovery of a molecular identifier for these selectively vulnerable cells gives us the opportunity to study in detail exactly why they succumb to tau pathology, and what could be done to make them more resilient.

“This would be a totally new and much more targeted approach to developing therapies to slow or prevent the spread of Alzheimer’s disease.”

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