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Libby and Tom Bates // CBS News

A brain disease best known for impacting football players who suffered concussions is now being found in soldiers

By Sharyn Alfonsi, September 16, 2018, CBS News

Until a few years ago, NFL players who struggled with severe depression, bouts of rage and memory loss in their retirement were often told they were just having a hard time adjusting to life away from the game. Doctors have since learned these changes can be symptoms of the degenerative brain disease CTE – chronic traumatic encephalopathy, caused by blows to the head.

As we first reported in January, CTE isn’t just affecting athletes, but also showing up in our nation’s heroes. Since 9/11 over 300,000 soldiers have returned home with brain injuries. Researchers fear the impact of CTE could cripple a generation of warriors.

When Joy Kieffer buried her 34-year old son this past summer, it was the end of a long goodbye.

Kieffer’s son, Sgt. Kevin Ash, enlisted in the Army Reserves at the age of 18. Over three deployments, he was exposed to 12 combat blasts, many of them roadside bombs. He returned home in 2012 a different man.

Joy Kieffer: His whole personality had changed. I thought it was exposure to all of the things that he had seen, and he had just become harder. You know, but he was — he was not happy.

Sharyn Alfonsi: So at this point, you’re thinking this decline, this change in my child is just that he’s been in war and he’s seen too much.

Joy Kieffer: Right.

Sharyn Alfonsi: Did he tell you about blasts that he experienced during that time?

Joy Kieffer: Uh-huh.

Sharyn Alfonsi: What did he–tell you?

Joy Kieffer: That they shook him. And he was having blackouts. And — it frightened him.

Ash withdrew from family and friends. He was angry. Depressed. Doctors prescribed therapy and medication, but his health began to decline quickly. By his 34th birthday, Sgt. Kevin Ash was unable to speak, walk or eat on his own.

Sharyn Alfonsi: Looking back on it now, was there anything you feel like he could’ve done?

Joy Kieffer: Uh-uh.

Sharyn Alfonsi: Because?

Joy Kieffer: Because it was– it– it was his brain. The thing I didn’t know was that his brain was continuing to die. I mean, before he went into the service he said, “you know, I could come back with no legs, or no arms, or even blind, or I could be shot, I could die,” but nobody ever said that he could lose his mind one day at a time.

His final wish was to serve his country one last time by donating his brain to science — a gesture he thought would bring better understanding to the invisible wounds of war.

Joy reached out to the VA-Boston University-Concussion Legacy Foundation Brain Bank where neuropathologist Dr. Ann McKee is leading the charge in researching head trauma and the degenerative brain disease CTE.

McKee has spent fourteen years looking at the postmortem brains of hundreds of athletes who suffered concussions while playing their sport.

Last summer, her findings shook the football world when she discovered CTE in the brains of 110 out of 111 deceased NFL players — raising serious concerns for those in the game today.

And when Dr. McKee autopsied Patriots tight-end Aaron Hernandez who killed himself after being convicted of murder, she found the most severe case of CTE ever, in someone under 30.

Now she’s seeing similar patterns in deceased veterans who experienced a different kind of head trauma — combat blasts. Of the 125 veterans’ brains Dr. Mckee’s examined, 74 had CTE.

Sharyn Alfonsi: I can understand a football player who keeps, you know, hitting his head, and having impact and concussions. But how is it that a combat veteran, who maybe just experienced a blast, has the same type of injury?

Dr. Ann McKee: This blast injury causes a tremendous sort of– ricochet or– or– a whiplash injury to the brain inside the skull and that’s what gives rise to the same changes that we see in football players, as in military veterans.

Blast trauma was first recognized back in World War I. Known as ‘shell shock,’ poorly protected soldiers often died immediately or went on to suffer physical and psychological symptoms. Today, sophisticated armor allows more soldiers to walk away from an explosion but exposure can still damage the brain — an injury that can worsen over time.

Dr. Ann McKee: It’s not a new injury. But what’s been really stumping us, I think, as– as physicians is it’s not easily detectable, right? It’s– you’ve got a lot of psychiatric symptoms– and you can’t see it very well on images of the brain and so it didn’t occur to us. And I think that’s been the gap, really, that this has been what everyone calls an invisible injury.

Dr. Ann McKee: This is the world’s largest CTE brain bank.

The only foolproof way to diagnose CTE is by testing a post-mortem brain.

Sharyn Alfonsi: So these are full of hundreds of brains…

Dr. Ann McKee: Hundreds of brains, thousands really…

Researchers carefully dissect sections of the brain where they look for changes in the folds of the frontal lobes – an area responsible for memory, judgement, emotions, impulse control and personality.

Dr. Ann McKee: Do you see there’s a tiny little hole there? That is an abnormality. And it’s a clear abnormality.

Sharyn Alfonsi: And what would that affect?

Dr. Ann McKee: Well, it’s part of the memory circuit. You can see that clear hole there that shouldn’t be there. It’s connecting the important memory regions of the brain with other regions. So that is a sign of CTE.

Thin slivers of the affected areas are then stained and viewed microscopically. It’s in these final stages where a diagnosis becomes clear as in the case of Sgt. Kevin Ash.

Sharyn Alfonsi: So this is Sergeant Ash’s brain?

Dr. Ann McKee: Right. This is– four sections of his brain. And what you can see is– these lesions. The, and those lesions are CTE And they’re in very characteristic parts of the brain. They’re at the bottom of the crevice. That’s a unique feature of CTE.

Sharyn Alfonsi: And in a healthy brain, you wouldn’t see any of those kind of brown spots?

Dr. Ann McKee: No, no, it would be completely clear. And then when you look microscopically, you can see that the tau, which is staining brown and is inside nerve cells is surrounding these little vessels.

Sharyn Alfonsi: And explain, what is the tau?

Dr. Ann McKee: So tau is a protein that’s normally in the nerve cell. It helps with structure and after trauma, it starts clumping up as a toxin inside the nerve cell. And over time, and even years, gradually that nerve cell dies.

Dr. Lee Goldstein has been building on Dr. McKee’s work with testing on mice.

Inside his Boston University lab, Dr. Goldstein built a 27-foot blast tube where a mouse – and in this demonstration, a model – is exposed to an explosion equivalent to the IEDs used in Iraq and Afghanistan.

Dr. Lee Goldstein: When it reaches about 25 this thing is going to go.

Dr. Goldstein’s model shows what’s going on inside the brain during a blast. The brightly colored waves illustrate stress on the soft tissues of the brain as it ricochets back and forth within the skull.

Dr. Lee Goldstein: What we see after these blast exposures, the animals actually look fine. Which is shocking to us. So they come out of what is a near lethal blast exposure, just like our military service men and women do. And they appear to be fine. But what we know is that that brain is not the same after that exposure as it was microseconds before. And if there is a subsequent exposure, that change will be accelerated. And ultimately, this triggers a neurodegenerative disease. And, in fact, we can see that really after even one of these exposures.

Sharyn Alfonsi: The Department of Defense estimates hundreds of thousands of soldiers have experienced a blast like this. What does that tell you?

Dr. Lee Goldstein: This is a disease and a problem that we’re going to be dealing with for decades. And it’s a huge public health problem. It’s a huge problem for the Veterans Administration. It’s a huge moral responsibility for all of us.

A responsibility owed to soldiers like 34-year-old Sgt. Tom Bates.

Sgt. Tom Bates: We were struck with a large IED. It was a total devastation strike.

Bates miraculously walked away from a mangled humvee — one of four IED blasts he survived during deployments in Iraq and Afghanistan.

Sharyn Alfonsi: Do you remember feeling the impact in your body?

Sgt. Tom Bates: Yes. Yeah.

Sharyn Alfonsi: What does that feel like?

Sgt. Tom Bates: Just basically like getting hit by a train.

Sharyn Alfonsi: And you were put back on the frontlines.

Sgt. Tom Bates: Yes.

Sharyn Alfonsi: And that was it?

Sgt. Tom Bates: Uh-huh

When Bates returned home in 2009, his wife Libby immediately saw a dramatic change.

Libby Bates: I thought, “Something is not absolutely right here. Something’s going on. For him to just lay there and to sob and be so sad. You know, what do you do for that? How do I– how do I help him? He would look at me and say, “If it wasn’t for you, I would end it all right now.” You know, I mean, like, what do you– what do you do– and what do you say to somebody who says that? You know I love this man so much. And —

Sharyn Alfonsi: You’re going to the VA, you’re getting help, but did you feel like you weren’t getting answers?

Sgt. Tom Bates: Yes.

Sharyn Alfonsi: And so you took it into your own hands and started researching?

Sgt. Tom Bates: I knew the way everything had gone and how quick a lot of my neurological issues had progressed that something was wrong. And I just– I wanted answers for it.

That led him to New York’s Mount Sinai Hospital where neurologist Dr. Sam Gandy is trying to move beyond diagnosing CTE only in the dead by using scans that test for the disease in the living.

Dr. Sam Gandy: By having this during life, this now gives us for the first time the possibility of estimating the true prevalence of the disease. It’s important to estimate prevalence so that people can have some sense of what the risk is.

In the past year, 50 veterans and athletes have been tested for the disease here. Tom Bates asked to be a part of it.

That radioactive tracer – known as t807 – clings to those dead clusters of protein known as tau, which are typical markers of the disease.

Through the course of a 20 minute PET scan, high resolution images are taken of the brain and then combined with MRI results to get a 360 degree picture of whether there are potential signs of CTE.

Scan results confirmed what Tom and Libby had long suspected.

On the right, we see a normal brain scan with no signs of CTE next to Tom’s brain where tau deposits, possible markers of CTE, are bright orange.

Dr. Sam Gandy: Here these could be responsible for some of the anxiety and depression he’s suffered and we’re concerned it will progress.

Sgt. Tom Bates: My hope is that this study becomes more prominent, and gets to more veterans, and stuff like that so we can actually get, like, a reflection of what population might actually have this.

There is no cure for CTE.

Dr. Gandy hopes his trial will lead to drug therapies so he can offer some relief to patients like Tom.

Dr. Ann McKee believes some people may be at higher risk of getting the disease than others.

While examining NFL star Aaron Hernandez’s brain she identified a genetic bio-marker she believes may have predisposed him to CTE.

A discovery that could have far-reaching implications on the football field and battlefield.

Sharyn Alfonsi: Do you think you will ever be your old self again?

Sgt. Tom Bates: I don’t ever see me being my old self again. I think it’s just too far gone.

Sharyn Alfonsi: So what’s your hope then?

Sgt. Tom Bates: Just to not become worse than I am now.

Since our story first aired, over 100 veterans have contacted Dr. Gandy to enroll in ongoing trials to identify whether they are living with CTE. And more than 300 have reached out to Dr. Mckee about donating their brains to research.

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Ann C. McKee, chief of neuropathology at the VA Boston Healthcare System, which houses the world’s largest brain bank devoted to CTE research, examines a brain earlier this month.(Photo: Robert Deutsch, USA TODAY)

Researchers close in on CTE diagnosis in living, one brain at a time

By Nancy Armour, August 24, 2018, USA TODAY

BOSTON – Submerged in chemicals in the stainless-steel bowl is the key to life and, researchers hope, death.

It’s a human brain. That of a man who played college football in the 1950s, to be exact. His family donated his brain to get answers for themselves, but what’s found could lead to more answers about chronic traumatic encephalopathy, the devastating neurodegenerative disease linked to concussions and repetitive head trauma from football and other contact sports.

“Our main objective, our overarching goal, is to help the people who are living. To be able to diagnose this disease during life,” says Ann McKee, chief of neuropathology at the VA Boston Healthcare System, which houses the world’s largest brain bank devoted to CTE research.

“If we can diagnose it, we can monitor it and test therapies to see if they’re effective in treating this disease,” says McKee, director of the CTE Center at Boston University’s School of Medicine. “It would really dramatically increase our ability to point out genetic susceptibilities for this. We’d be able to look at how much is too much in certain individuals or certain positions in certain sports.”

As another football season begins, it inevitably leads to questions and fears about head trauma and its long-term damage. How many hits are too many? What can parents do to protect their children or players do to protect themselves? Are athletes in certain sports more susceptible?

Most important, which athletes will develop CTE – or Parkinson’s or ALS (amyotrophic lateral sclerosis) – and why?

The answers will come from brains such as the one McKee dissected this month, when USA TODAY Sports toured the brain bank.

The brain bank has more than 500 brains, most of them donated by former athletes or their families who suspected CTE because of mood swings, behavioral changes, depression or dementia. Of those brains, more than 360 had CTE, McKee says.

SEARCHING FOR CLUES

The arrival of a brain sets two teams in motion. One set of clinicians talks to the family to find out more about the donors. Did they play any sports? If so, what and for how long? When did they start? Did they experience any other kind of head trauma, say from an automobile accident, domestic violence or military service? Did they have drug or alcohol problems? How did their mental health change, and when did that occur?

Separately, and usually without any information about the person whose brain it was, McKee and her researchers study the brain. It is cut in half, and one half is stored in a minus-80-degree freezer, so it will be available for molecular, genetic and biochemical studies.

The other half is then photographed and sectioned. After removing the brain stem, McKee uses what looks like a bread knife to cut slices of the brain about a quarter-inch thick.


Ann C. McKee slices the brain into segments about a quarter-inch thick as part of in-depth, time consuming research on the organ. McKee hopes the work will unlock answers to CTE. (Photo: Robert Deutsch, USA TODAY)
 
Simply by looking at the brain, McKee can tell a few things. The brain of this man, who was in his 80s when he died, has shrunk, noticeably smaller than it should be for a man who once played football. The folds of the brain, normally pressed tightly against one another, are loose and have gaps between them, some large enough that the tip of a finger could be inserted.

She points to the ventricles, chambers in the middle of his brain that are filled with fluid during life. They should be small, but these are “just gigantic.”

“As the brain shrinks, they expand. What this indicates is there’s been enormous shrinkage of the brain,” McKee says. “Those are huge.”

The hippocampus, a section in the middle of the brain that controls memory, is small but not abnormally so for a man in his 80s. If it was, that could be an indication of Alzheimer’s. But a membrane that runs from one side of the brain to the other, normally thick like a rubber band, has shrunk. In some spots, it’s almost invisible.

“This is looking more like frontal predominant atrophy, and that could mean CTE because Alzheimer’s almost always affects the hippocampus,” McKee says. “At this point, I always want to know, ‘What is it? Let’s look under the microscope.’ But you have to wait.”

CTE can’t be seen by the naked eye, and it takes at least three weeks to prepare slides of the brain tissue.


 
CTE is caused by tau, a protein in the brain released as a result of head trauma. When tau clumps together, it damages brain cells and can change the brain’s function. Though tau causes Alzheimer’s, McKee says, the tau that causes CTE looks distinctly different.

Under a microscope, it can be seen in telltale brown spots.

“CTE is very focal. In fact, in its early stages, it’s in the crevices. It just piles up. And that’s around blood vessels,” McKee says. “That’s very different. Alzheimer’s never does that.”

As CTE progresses, those clusters or clumps of tau will spread, and the disease will become more severe. That’s why, in the early stages of disease, stages 1 and 2, the symptoms usually relate to behavioral changes or mood swings. In stages 3 and 4, the disease is exhibited in memory loss.

“We think there may be more pathology in the young players than we’re appreciating just with the tau protein,” McKee says. “We think there’s maybe white matter structural changes or maybe inflammatory changes that are responsible for that loss of control, which is so difficult for the individuals.”

‘EVERY CASE IS A MYSTERY’

Once the slides have been examined, the pathologists and clinicians will come together for a conference. At this point, neither knows what the other does. The clinicians detail what they’ve learned about the brain donor’s history and suggest a diagnosis. The pathologists will then say whether the brain tissue confirms it.

“Every case is a mystery,” McKee says. “It’s not the same way you usually solve a mystery. I solve the pathology first, and then you go back and find out (the history). And then you try and put the two together.”

Some former players and their families once were reluctant to donate their brains, but that stigma largely has disappeared. So much so that McKee said brains arrive at the Boston bank almost every day.

Though that lengthens the time it takes to reach a definitive diagnosis, it will shorten the time before a living diagnosis can be found. In addition to the work done in her lab, McKee shares tissue samples with researchers around the world.

“What we want to do is establish the risk, educate people, educate parents, educate players,” McKee says. “So if they’re unwilling to risk that future self, if they’re unwilling to take that risk because it’s too high for them personally, we want to give them enough data so they can make a very sound and wise decision.”

When that day comes, it will change sports forever.

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Traumatic brain injury causes widespread damage to neurons, leading to deficits in learning and memory. Cypin activators restore neuronal survival and function in mice, allowing for normal learning and memory. Credit: Mihir Patel/Rutgers University-New Brunswick

Traumatic brain injury: Discovery of two molecules could lead to new drug treatments

By Todd B. Bates, July 27, 2018, Rutgers University

After 10 years of research, a Rutgers-led team of scientists has identified two molecules that protect nerve cells after a traumatic brain injury and could lead to new drug treatments.

The molecules promote full recovery after traumatic brain injury (TBI) in mice, according to the study published online in Neurobiology of Disease. Traumatic brain injury is the leading cause of death for people under 45 years old in the United States and is associated with disability, early-onset dementia, cognitive disorders, mental illness and epilepsy.

Nearly all approaches for treating TBI focus on trying to prevent neurons, or nerve cells, from degenerating or on attempting to promote their survival, the study notes. TBI typically alters neural circuits within injured brain regions.

“The big issue with treatment after TBI is that there are no drugs that work well on patients to restore memory, and we’re targeting reconnectivity of neural circuitry,” said Bonnie L. Firestein, senior author of the study and a professor in the Department of Cell Biology and Neuroscience at Rutgers University-New Brunswick. “That means we want our neurons to function properly and connect with other neurons. We want to allow people to retain their cognition and ability to remember and learn, so our angle is novel.”

The researchers studied the protein cypin, an enzyme that breaks down guanine, which is an important building block for DNA and RNA in cells. The scientists previously showed that cypin is involved in promoting the proper shape in neurons and “keeping them happy,” Firestein said. This study found that speeding the breakdown of guanine protects neurons from injury and retains brain functioning.

Scientists at Rutgers-New Brunswick, University of Pennsylvania, Fox Chase Chemical Diversity Center Inc. and Columbia University want to develop drugs from the molecules for further studies.

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With better devices, science can get closer to a more complete picture of how neurons interact for cognitive functionality. (Photo/iStock)

Are we getting closer to a complete brain mapping? New devices explore more regions safely

By Breanne Grady, April 13, 2018, viterbischool.usc.edu

Researchers have developed thin, flexible polymer-based materials that record activity in more subregions of the brain with safer, more specific placement.

Science has yet to unravel a complete understanding of the brain and all its intricate workings. It’s not for lack of effort.

Over many decades, multiple research studies have sought to understand the dizzying “talk,” or interconnectivity, between thousands of microscopic entities in the brain, in particular neurons. The goal: to one day arrive at a complete brain “mapping” — a feat that could unlock tremendous therapeutic potential.

Researchers at the USC Viterbi School of Engineering have developed thin, flexible polymer-based materials for use in microelectrode arrays that record activity more deeply in the brain and with more specific placement than ever before. What’s more is that each microelectrode array is made up of eight “tines,” each with eight microelectrodes which can record from a total 64 subregions of the brain at once.

Same Quality, More Safety

In addition, the polymer-based material, called Parylene C, is less invasive and damaging to surrounding cells and tissue than previous devices comprised of silicon or microwires. However, the long and thin probes can easily buckle upon insertion, making it necessary to add a dissolvable brace made up of polyethylene glycol (PEG) that prevents it from bending.

Professor Ellis Meng of the USC Viterbi Department of Biomedical Engineering said that the performance of the new polymer-based material is on par with microwires in terms of recording fidelity and sensitivity. “The information that we can get out is equivalent, but the damage is much less,” Meng said. “Polymers are gentler on the brain, and because of that, these devices get recordings of neuronal communication over long periods of time.”

As with any prosthetic implant, caution must be exercised in terms of the body’s natural immune response to a foreign element. In addition to inflammation, previous microelectrode brain implants made of silicon or microwires have caused neuronal death and glial scarring, which is damage to connective tissue in the nervous system. However, Parylene C is biocompatible and can be microfabricated in extremely thin form to mold well to specific subregions of the brain, allowing for exploration with minimal damage.

Listening In

So far, these arrays have been used to record synaptic responses of individual neurons within the hippocampus, a part of the brain responsible for memory formation. If injured, the hippocampus may be compromised, resulting in a patient’s inability to form new memories. Meng, a faculty member of the Michelson Center for Convergent Bioscience, said that the polymer-based material can conform to a specific location in the hippocampus and “listen in on a conversation” between neurons. Because there are many such “eavesdroppers” (the microelectrodes), much more information about their interconnectivity can be gleaned.

“I can pick where I want my electrodes to be, so I can match up to the anatomy of the brain,” Meng, the Dwight C. and Hildagarde E. Baum Chair, said. “Along the length of a tine, I can put a group of electrodes here and a group of electrodes there, so if we plant to a certain depth, it’s going to be near the neurons I want to record from.”

Up Next

Future research will determine the recording lifetime of polymer-based arrays and their long-term “signal-to-noise” (SNR) stability. Also, the team plans to create devices with even higher density, including a double-sided microelectrode array with 64 electrodes per tine instead of eight — making for a total of around 4,000 electrodes placed in the brain at once.

In addition to Meng, Professor Ted Berger, the David Packard Chair in Engineering, and Research Professor Dong Song (both of the USC Viterbi School of Engineering) were co-authors along with Ph.D. students Huijing Xu and Ahuva Weltman Hirschberg and post-doctoral scholar Kee Scholten. Funding was provided be the National Science Foundation (NSF) and the National Institutes of Health (NIH). The study titled “Acute in vivo testing of a conformal polymer microelectrode array for multi-region hippocampal recordings” now published in the Journal of Neural Engineering.

About the Michelson Center

The USC Michelson Center for Convergent Bioscience brings together a diverse network of premier scientists and engineers under one roof, thanks to a generous $50 million gift from orthopedic spinal surgeon, inventor and philanthropist Gary K. Michelson, and his wife, Alya Michelson. At the Michelson Center, scientists and engineers from the USC Dornsife College of Letters, Arts and Sciences, USC Viterbi School of Engineering and Keck School of Medicine of USC are working to solve some of the greatest intractable problems of the 21st century in biomedical science, including a fundamentally new understanding of the cell and new approaches for cancer, neurological and cardiovascular disease.

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New app designed to help survivors of traumatic brain injury recognize and regulate emotions

Indiana University School of Medicine, May 8, 2018

A new app developed by an Indiana University School of Medicine faculty member is designed to help survivors of traumatic brain injuries recognize and regulate their emotions— skills that are critical to maintaining relationships and quality of life but that are often compromised in patients who have endured head traumas.

The app, called My Emotional Compass, is the result of years of research led by Dawn M. Neumann, PhD, associate professor of physical medicine and rehabilitation at IU School of Medicine and research director at the Rehabilitation Hospital of Indiana. It is available on the Apple App Store and the Google Play Store.

Patients with TBI frequently experience damage to regions of the brain and neural networks involved with processing emotions. As a result, many survivors have trouble identifying, labeling and expressing their emotions, a condition known as alexithymia. For example, patients may be unable to articulate that receiving a surprise gift made them feel happy and appreciative, or that being passed over for a promotion left them feeling frustrated and ashamed.

As many as 60 percent of individuals with moderate to severe TBI experience alexithymia, making it challenging to display empathy and respond in a socially appropriate manner in personal and professional relationships. Patients with mild TBI also experience this challenge.

There are no standard, evidenced-based interventions to treat these issues. The app and related research studies led by Neumann aim to begin filling this gap. My Emotional Compass is specifically designed to address alexithymia by helping patients interpret and put words to their own feelings.

“We need to re-teach individuals who have experienced a traumatic brain injury about emotions and give them an emotional vocabulary,” Neumann said. “It might sound simplistic, but the very act of labeling an emotion can help control it.”

In addition to problems with recognizing and labeling personal emotions, many patients with TBI also have difficulty recognizing others’ emotions, interpreting tone of voice, reading facial and physical cues, and responding empathetically to these cues. “You can’t understand what it means that someone else is feeling sad or angry if you don’t recognize those emotions in yourself,” Neumann said.

Because there is an association between recognizing self-emotions and recognizing and responding to others’ emotions, there is a possibility treatments aimed at reducing alexithymia may also improve these other related skills as well.

The app takes users through a series of questions and helps them identify how they are feeling in response to certain scenarios. For example, a user is asked to think of a situation that occurred earlier in the day, then to identify if the experience was pleasant or unpleasant, and to further refine the emotional response in terms of level of emotional charge. (Did the event elicit a strong, moderate or mild emotional arousal?) This ultimately guides the individual to understand the nuances between feelings of anxiety, fear, disgust or anger, for instance.

The app is based on a pilot study led by Neumann at the Rehabilitation Hospital of Indiana that employed the same techniques. It involved patients who, on average, had experienced a traumatic brain injury at least eight years prior. They underwent eight, one-hour emotional awareness training sessions with a research therapist. The results were promising. “We have patients who benefitted tremendously, and the benefits were lasting,” Neumann said.

After the trial, patients were given a laminated piece of paper that reinforced what they learned and served as their Emotional Compass. Neumann sought to make the tool available to a broader audience in a user-friendly format. She selected CreateAbility Concepts, Inc. to help develop the app because of the company’s understanding of this population. It helped transfer Neumann’s manual compass into a highly interactive app through an elaborate series of interviews and mock-ups.

CreateAbility Concepts licensed Neumann’s work through the IU Innovation and Commercialization Office, which protects, markets and licenses intellectual property developed at Indiana University so it can be commercialized by industry.

“This license agreement is a perfect marriage of Dawn Neumann’s outstanding content and CreateAbility Concept’s superior technical know-how,” said David Wilhite, director at ICO. “We are glad to license this intellectual property to an Indiana-based company to bring it to the market.”

Patients are encouraged to use My Emotional Compass in collaboration with a clinician, such as a psychologist or speech language pathologist.

“The inability to recognize and interpret emotions puts a significant strain on relationships and impedes a person’s quality of life, but it is a problem that is often overlooked as clinicians focus on immediate and long-term physical complications of the injury,” Neumann said. “My hope is that this app continues to shine a light on the importance of treating alexithymia and other related conditions and empowers patients by giving them access to an effective, easy-to-use tool.”

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The radial-arm water maze is a common test to assess working memory in rodents.

Memory-enhancing drug reverses effects of traumatic brain injury in mice

By Ryan Cross, Jul. 10, 2017, sciencemag.org

Whether caused by a car accident that slams your head into the dashboard or repeated blows to your cranium from high-contact sports, traumatic brain injury can be permanent. There are no drugs to reverse the cognitive decline and memory loss, and any surgical interventions must be carried out within hours to be effective, according to the current medical wisdom. But a compound previously used to enhance memory in mice may offer hope: Rodents who took it up to a month after a concussion had memory capabilities similar to those that had never been injured.

The study “offers a glimmer of hope for our traumatic brain injury patients,” says Cesario Borlongan, a neuroscientist who studies brain aging and repair at the University of South Florida in Tampa. Borlongan, who reviewed the new paper, notes that its findings are especially important in the clinic, where most rehabilitation focuses on improving motor—not cognitive—function.

Traumatic brain injuries, which cause cell death and inflammation in the brain, affect 2 million Americans each year. But the condition is difficult to study, in part because every fall, concussion, or blow to the head is different. Some result in bleeding and swelling, which must be treated immediately by drilling into the skull to relieve pressure. But under the microscope, even less severe cases appear to trigger an “integrated stress response,” which throws protein synthesis in neurons out of whack and may make long-term memory formation difficult.

In 2013, the lab of Peter Walter, a biochemist at the University of California, San Francisco (UCSF), discovered a compound—called ISRIB—that blocked the stress response in human cells in a dish. Surprisingly, when tested in healthy mice, ISRIB boosted their memory. Wondering whether the drug could also reverse memory impairment, Walter teamed up with UCSF neuroscientist Susanna Rosi to study mouse models of traumatic brain injury. First, they showed that the stress response remains active in the hippocampus, a brain region important for learning and memory, for at least 28 days in injured mice. And they wondered whether administering ISRIB would help.

Rosi and her team first used mechanical pistons to hit anesthetized mice in precise parts of their surgically exposed brains, resulting in contusive injuries, focused blows that can also result from car accidents or being hit with a heavy object. After 4 weeks of rest, Rosi trained the mice to swim through a water maze, where they used cues to remember the location of a hidden resting platform. Healthy mice got better with practice, but the injured ones didn’t improve. However, when the injured mice were given ISRIB 3 days in a row, they were able to solve the maze just as quickly as healthy mice up to a week later, the researchers report today in the Proceedings of the National Academy of Sciences.

“We kept replicating experiments, thinking maybe something went wrong,” Rosi says. So the team decided to study ISRIB in a second model of traumatic brain injury known as a closed head injury, which resembles a concussion from a fall. They again used a mechanical piston, but this time landed a broad blow to the back of the skull. Two weeks later, the mice were trained on a tougher maze, full of bright lights and loud noise. They had to scurry around a tabletop with 40 holes, looking for the one with an escape hatch. Again, while the uninjured mice improved at the task, the concussed mice never got the hang of it. But after four daily doses of ISRIB, the concussed mice performed as well as their healthy counterparts. “This is the most exciting piece of work I’ve ever done, no doubt,” Rosi says.

“Paradigm shift is not too strong a term to use,” says Ramon Diaz-Arrastia, neurologist and director of clinical traumatic brain injury research at the University of Pennsylvania. “This … shows for the first time that a therapy in the chronic period of traumatic brain injury can have pretty potent effects.” Walter agrees. “Normally you would give up on these mice and say nothing can be done here,” he says. “But ISRIB just magically brings the cognitive ability back.”

Still, Borlongan cautions that studies in animals often don’t pan out when tested in humans. He says that this drug has a leg up, though, because it was tested in two models and also readily crosses the blood-brain barrier, which prevents many drugs that look good on paper from entering the brain and having an effect.

If the therapy translates to humans, it could be a boon for soldiers returning from war, who sometimes wait weeks between leaving the battlefield and arriving home for treatment. Brian Head, a neurobiologist at the VA San Diego Healthcare System in California notes that traumatic brain injury is still hard to diagnose, especially with veterans that show up to the clinic long after the injury. “But right now nothing else is working, and giving a compound [that works] a month later is really impressive.”

In 2015, ISRIB was licensed to the secretive Google spinout company Calico, which studies the biology of aging and life span. Walter says his lab has a research agreement with Calico to pursue “basic mechanistic work” on ISRIB, but that the new study was not funded by Calico. Google declined to comment on the new research.

Although the protein target of ISRIB is known, the exact manner in which the drug restores memory is hazy. The team hypothesizes that ISRIB may work by allowing normal protein synthesis—essential for making new neuronal connections and thus forming new memories—to resume, which would otherwise be blunted by the integrated stress response. “Even if this drug doesn’t materialize, other ways of manipulating the integrated stress response may lead to an effective treatment in the future,” Walter says.

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CARSON, CA – AUGUST 03: Bronze medal winner Dave Mirra speaks in a press conference after the Rally Car race during the summer X Games 14 at Home Depot Center on August 3, 2008 in Carson, California. (Photo by Christian Petersen/Getty Images)

Months after committing suicide, Dave Mirra has become the first action sports athlete to be diagnosed with CTE

by Robert Silverman, vocativ.com (May 24, 2016)
 
After BMX biking legend Dave Mirra committed suicide on February 4 of this year, his wife had his brain tested for chronic traumatic encephalopathy. Sadly, the result came back positive, rife with tau proteins dotting both his temporal and frontal lobes after years of enduring an unknown amount of concussive and sub-concussive trauma. This makes Mirra the first action sports athlete to be diagnosed with CTE.

The neuropathologist went so far as to equate the condition of his brain to that of NFL players and other contact sport athletes that have been posthumously diagnosed with the disease. “I couldn’t tell the difference,” Dr. Lili-Naz Hazrati said.

In an exclusive interview with ESPN: The Magazine, Mirra’s wife Lauren describes the agonizing final weeks of his life, the transformation of his formerly vibrant personality into something different and darker, prone to wild mood swings and unprovoked crying jags or bouts of exhaustion, his mind clouded and wracked with depression.

“I remember seeing him sitting on our bed one day, in the last month of his life,” she said. “I had just gotten out of the shower and saw him hunched over with the blankest lost look. I sat down next to him and held his hand. I said, ‘What is wrong? Are you OK?’ And he just shrugged his shoulders. He couldn’t even speak. He didn’t know. He couldn’t put it into words. He was lost. He was helpless. It was completely different from who he was.”

“He was gone. I could see straight through him,” she continued. “It was the hardest thing to see, looking at someone you love, and you can’t have a conversation with them, and you can see straight through their eyes.”

Lauren Mirra doesn’t know what her exact plans might be for the future, but her overarching hope is that she’ll be able to find a forum in which to speak out, to encourage best practices and prevention measures, without coming across as an ideologue out to ban action sports altogether.

“Through him we have an opportunity to help and change,” she said. “Beauty from ashes. That’s how I will always choose to see it.”

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The Cohen family partners with USC to serve families in Los Angeles.
 
by Lynn Lipinski, tfm.USC.edu (Autumn 2016) — PEACE AFTER WAR can be elusive for combat veterans who fight painful memories long after they’ve left the battlefield. Of the more than 2.6 million men and women who have served in the U.S. military since 9/11, about 20 percent experience some form of post-traumatic stress or brain injury—but nearly half forego treatment, according to the Cohen Veterans Network.

The Steven A. Cohen Military Family Clinic at USC, made possible by a $15.7 million gift from Steven Cohen and the Cohen Veterans Network, offers veterans and their family members free outpatient mental health services and case management. Recently opened in downtown Los Angeles, the Cohen Military Family Clinic at USC is part of a national network of clinics serving veterans and is a collaboration between the USC School of Social Work and the Keck School of Medicine of USC.

Providers will also be stationed at locations throughout the county in areas that otherwise lack these types of services. The clinic will also serve veterans who are ineligible for Veterans’ Admnistration benefits, such as those who served in the National Guard or the Reserves.

“The wounds of war are serious. It is not easy to serve your country in combat overseas and then come back into society seamlessly, especially if you are suffering,” says Cohen, chairman and CEO of Point72 Asset Management. “Veterans have paid an incredible price. It’s important that this country pays back that debt.”

The Cohen Veterans Network plans to create a system of about two dozen centers across the country by 2020 as part of a $275 million initiative to improve access to behavioral health care for recent veterans. Cohen’s support of services for veterans began in part because of a personal connection: His son, Robert, deployed to Afghanistan with the Marines and is currently in the Reserves.

USC’s strong programs for veterans made it a natural fit to host the clinic. The USC School of Social Work is home to the Center for Innovation and Research on Veterans and Military Families, where researchers conducted the first comprehensive study of veterans in L.A. County. Their findings are already helping to create effective services for veterans. The school has also earned national recognition for its pioneering master’s degree in military social work—the only program of its kind offered by a civilian research university.

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By Alyssa Navarro, Tech Times (August 23, 2016) — Federal health regulators in the United States approved on Monday the use of two new computer softwares as cognitive screening tests for traumatic head injury patients.

Known as ImPACT or the Immediate Post-Concussion Assessment and Cognitive Testing (ImPACT), the new testing device, as well as a similar test designed for children, can be used by doctors to evaluate signs and symptoms of head injuries that could indicate concussion.

ImPACT is designed for patients aged 12 to 59 years old, while ImPACT Pediatric is intended for children aged 5 to 11 years old, officials said. Licensed health care professionals are the only ones allowed to perform the analysis and interpret the results.

The software can be accessed easily because it runs on both desktop computers and laptops, according to the U.S. Food and Drug Administration (FDA). Both tests the first ever devices permitted by the FDA to assess cognitive function after experiencing a possible concussion. They are designed to be part of medical evaluations in hospitals.

Although ImPACT and ImPACT Pediatric will definitely be useful for doctors, both tests are not meant to diagnose concussions or determine treatments that are appropriate for such cases, the FDA said.

Instead, both devices are only designed to test cognitive skills such as reaction time, memory and word recognition. All of these can be impacted by head injuries. Afterwards, the results are compared to a patient’s pre-injury baseline scores or an age-matched control database, the FDA said.

Dr. Carlos Peña, director of the neurological and physical medicine division at the Center for Devices and Radiological Health, acknowledges that the two testing devices can provide useful information that can aid doctors in the evaluation of people who are experiencing potential signs of concussion.

However, Peña says that clinicians should not completely depend on the tests alone to rule out concussion or to decide whether a player with a head injury should return to a game.

Statistics from the Centers for Disease Control and Prevention (CDC) reveal that traumatic brain injuries are responsible for more than 2 million visits to the emergency room in the country annually. Traumatic brain injuries also account for more than 50,000 deaths in America every year.

Cases of head injury among kids have been increasing. In May, a CDC report showed that from January 2001 to December 2013, approximately 214,883 children aged 14 years old and below were brought to emergency departments due to head injuries.

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When a person has a stroke, blood flow to the brain is interrupted, causing brain cells to die within minutes due to lack of oxygen. In some cases, this can result in paralysis, speech and language problems, vision problems, and memory loss. But in a new study, researchers have shown that stem cell therapy increases nerve cell production in mice with brain damage due to stroke.

by Marie Ellis, MedicalNewsToday.com (August 22, 2016) — The researchers – led by Berislav Zlokovic, M.D., Ph.D., from the University of Southern California (USC) – publish their findings in the journal Nature Medicine.

According to the Centers for Disease Control and Prevention (CDC), stroke is the fifth leading cause of death in the United States and is also a major cause of disability in adults.

The effects of a stroke depend on the location of the blockage and how much brain tissue is involved, but a stroke on one side of the brain will result in neurological effects on the opposite side of the body.

For example, a stroke on the right side of the brain could produce paralysis on the left side of the body, and vice versa.

A stroke in the brain stem can affect both sides of the body and could leave the patient in a so-called locked-in state, where the patient is unable to speak or move the body below the neck.

Given that about 800,000 people in the U.S. have a stroke each year, the researchers of this latest study wanted to investigate potential therapies.

Therapy is a combination of two methods

The researchers say their therapy is a combination of two methods. One involves surgically grafting human neural stem cells onto the damaged area, where they are able to mature into neurons and other brain cells.

The other therapy uses a compound called 3K3A-APC, which has been shown to help neural stem cells that have been grown in a petri dish grow into neurons. But the researchers say it was not clear what effect the molecule – called activated protein-C (APC) – would have on live animals.

As such, the team used mice for their experiment, and they found that a month after inducing stroke-like brain damage in the mice, those that had received both the stem cells and 3K3A-APC performed much better on motor and sensory function tests, compared with mice that received only one of the treatments or neither.

The researchers also observed that the mice given 3K3A-APC had more stem cells survive and mature into neurons.

But how did the researchers induce stroke-like brain damage in the mice? They disrupted blood flow to a specific brain area.

Then, 1 week later, which is the mouse equivalent of several months in humans, the researchers inserted the stem cells next to the dead tissue and administered either a placebo or 3K3A-APC.

“When you give these mice 3K3A-APC, it works much better than stem cells alone,” says Dr. Zlokovic. “We showed that 3K3A-APC helps the cells convert into neurons and make structural and functional connections with the host’s nervous system.”

‘No one in the stroke field has ever shown this’

The researchers also looked at the connections between the neurons that grew from the stem cells in the damaged brain region and nerve cells in the primary motor cortex.

The team found that the mice given the stem cells and 3K3A-APC had more neuronal connections – synapses – that linked those areas, compared with the mice given the placebo.

Then, when the researchers stimulated the mice’s paws with a vibration, the neurons that grew from the stem cells exhibited a stronger response in the mice that were treated.

“That means the transplanted cells are being functionally integrated into the host’s brain after treatment with 3K3A-APC. No one in the stroke field has ever shown this, so I believe this is going to be the gold standard for future studies.” ~Dr. Berislav Zlokovic

Following on from this study, the researchers want to pursue another phase II clinical trial to examine whether the treatment combination can encourage the growth of new neurons in human stroke patients to improve function.

They say that if that trial is successful, it could be possible to test the therapy’s effects on other conditions, including spinal cord injuries.

“This USC-led animal study could pave the way for a potential breakthrough in how we treat people who have experienced a stroke,” says Jim Koenig, Ph.D., program director at the National Institute of Health’s National Institute of Neurological Disorders and Stroke (NINDS), who funded the study.

“If the therapy works in humans,” he adds, “it could markedly accelerate the recovery of these patients.”

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