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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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Junior Seau, shown at his beloved Pacific Ocean in the ESPN Films “30 for 30” documentary “Seau,” which premieres Thursday. (ESPN Films)

ESPN hits the mark with documentary ‘Seau’

By Tom Krasovic, September 20, 2018, San Diego Union Tribune

An aerial view of the Oceanside coast, in full sparkle and splendor below, grandly eases viewers into “Seau,” an ESPN Films documentary in the “30 for 30” series that debuts Thursday on the streaming service ESPN+.

It’s a sunny scene, the Pacific Ocean’s turquoise waves illuminated as they roll toward the white beach. The late Junior Seau told friends he found peace paddling on these waters, deep into his life alongside the town where he’d grown up.

Up at dawn with a yellow long-board and oar in hand, Seau had only a short walk from his beachfront home to the water.

Yet the former Chargers linebacker, role model and local philanthropist was then also writing in a journal of bouts with depression, memory loss and perceived guilt. There were headaches, too, and nights plagued by insomnia. “Buddy,” he’d told a friend and professional soccer player who’d suffered a brain injury from heading a ball, “I’ve had a concussion since I was 15.”

Diary entries also revealed feelings of humiliation and embarrassment over not living up to expectations of others and himself, and of feeling used by others.

“The world has nothing for me,” Seau pens in one entry, the cursive words all too legible.

One of Seau’s surviving adult children, after reading the grim line aloud, wonders why his father didn’t regard his family as something in this apparent world of nothing.

Why couldn’t they have been a lifeline for him to reach out and grasp?

“Seau,” produced and directed by Kirby Bradley, lets viewers draw their own conclusions about a complicated life that ended one May morning six years ago, at age 43, with a self-inflicted gunshot wound to the chest, but not before we hear from an array of family members, friends and experts in football and brain science.

At the end of the 90-minute film, themes of redemption and hope are raised.

“Let’s all walk from here being better for having known Junior Seau and the impact he had on our lives,” NFL quarterback Drew Brees, a former Chargers teammate of the Hall of Fame linebacker, concludes near the film’s end.

Former Chargers lineman Aaron Taylor notes that in death, Seau drew extraordinary attention to the link between head trauma and a degenerative brain disease, CTE, revealed in a tissue sample sent to a brain scientists at the family’s request.

Exciting beginnings and success are a thread to the film, followed often by bitter detours or hurtful endings.

Seau took to sports at Oceanside High with a passion that rivaled his stunning blend of size, speed and agility. If he was slamming into football ball-carriers or catching passes, scoring baskets or throwing the discus and shot, he was a “force of nature” for the green-and-white-clad Pirates, observers said.

A flood of football scholarship offers came to the small home where Seau and his brothers slept in a tiny garage.

Jubilation ensued when Seau chose USC, keeping him close to his parents and siblings and the tight-knit Samoan-American community in Oceanside. A similar celebration arose in 1990 when the Chargers drafted him fifth overall. “I’m a real momma’s boy,” Seau said, pulling on a blue team cap.

Playing for his beloved “Diego,” he led the long-struggling Chargers to the playoffs in just his third season, and their first Super Bowl two years later. “Now the world is gonna know the San Diego Chargers,” he told some 70,000 celebrants in Mission Valley after the team returned from claiming the 1994 AFC title in Pittsburgh.

The flip side?

If Oceanside lost a game in which he played, Junior lost his lunch money. It was the price his father exacted.

The thrill of signing with USC gave way to humiliation when a failed admittance test made him ineligible as a freshman. His father refused to talk to him in response, deeming the failure an embarrassment to the family. After a dominant junior year with USC, there would be no senior year. Making money was the next step, in no small part because he wanted to support his parents and other family members.

The Chargers couldn’t build upon their Super Bowl season, and the team’s constant losing wore on Seau.

When the Chargers traded him in the spring of 2003, after 13 seasons with the club, Seau was hurt that the team — Stay Unclassy, San Diego? — called not him but his agent to tell him the news. “I know that was hard on him,” said the agent, Steve Feldman.

Gina Seau was working for the Chargers in marketing when she first met Seau early in his NFL career.

She recalled “very kind eyes” and a “very soft voice” that almost “didn’t match the size and stature.”

The two would marry, but erratic behavior that Gina Seau linked to numerous football-related head injuries — “My head is on fire,” he told her — led to a divorce in 2002. The two remained friends. Believing that driving off a steep coastal cliff in October 2010 wasn’t an accident, Gina pleaded with her former husband to get help.

Here’s hoping that if there’s a “Seau II,” events yet to transpire bring more developments of redemption. Say, a cure for CTE.

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TIAA-CREF Tuition Financing, Inc. also Oversees Treasurer’s ScholarShare Program

August 8, 2018 | Contact:Press Office, news@sto.ca.gov, 916-653-2995

SACRAMENTO – California State Treasurer John Chiang today announced the selection of TIAA-CREF Tuition Financing, Inc. (TFI) to administer the California Achieving a Better Life Experience (CalABLE) Program.

“TFI’s selection means we’re one step closer to turning on CalABLE’s ‘Open for Business’ sign,” said State Treasurer John Chiang. “TFI’s expertise and oversight are a welcome help in reaching Californian’s with disabilities and their families, who will soon be able to save up to $15,000 a year, tax free, without jeopardizing their federal and state assistance.”

Currently, savings for individuals receiving Supplemental Security Income (SSI) or other public benefits have a $2,000 resource limit. Once a beneficiary is determined to have more than this $2,000, their benefits may be suspended until savings fall below that level. CalABLE — the state’s version of the federal ABLE Act — allows people with disabilities to establish a tax-advantaged savings account in which they can save up to $15,000 per year, up to a total of $100,000, without jeopardizing their ability to continue to receive existing public benefits. Earnings into CalABLE accounts are not subject to federal income tax or California state income tax, so long as the earnings are spent on a broad range of disability related expenses.

“We are excited to see the CalABLE program move forward in providing people with disabilities the opportunity to build their futures,” added Christina Mills, executive director of the California Foundation for Independent Living Centers. “There are very few ways for people in our community to save money without penalties. Opening a CalABLE account will be a game-changer for individuals with disabilities, and parents of children with disabilities, who have been limited by programs and services that prevent us from saving and becoming more independent.”

TFI was selected to manage the new CalABLE program by a vote on Tuesday by the CalABLE Act Board, based on the firm’s low costs, proposed investment portfolio that offered simple choices for enrollees with clear preferences, and the simplicity of its program for those new to such a savings program.
TFI is a national leader in providing program management services for college savings plans and currently serves as the manager for California’s successful ScholarShare 529 college savings program.

Any individual whose disability occurred before age 26 is eligible to open a CalABLE account so long as they receive benefits based on disability, such as SSI or Social Security Disability Insurance, or if they have disability certification (including a copy of a diagnosis signed by a physician).

CalABLE participants can:
• Make automatic contributions from a bank account
• Invite family and friends to contribute directly to an account
• Deposit online or by check
• Select from easy to understand investment options

Chiang added, “No one should have to fear losing their disability benefits because they decided to save wisely and invest in their future. This program will help ensure no Californian with a disability will be penalized for thinking ahead.”
CalABLE will launch by the end of 2018.

For more information about CalABLE visit https://www.treasurer.ca.gov/able or call 916-653-1728.

For more news, please follow the Treasurer on Twitter at @CalTreasurer, and on Facebook at California State Treasurer’s Office

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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The Intrepid Spirit traumatic brain injury treatment center is slated to open April 2 at Camp Pendleton. (Courtesy Naval Hospital Camp Pendleton) (Photo/iStock)

Brain injury center to open at Marine base

By Linda McIntosh, March 27, 2018, sandiegouniontribune.com

A brain injury treatment center for military personnel will open its doors April 2 near the Naval Hospital Camp Pendleton.

The $11.5 million Intrepid Spirit center is the seventh of nine such facilities at military bases across the country. It is funded by the New York-based nonprofit Intrepid Fallen Heroes Fund founded in 2000 by Zachary Fisher, who also started the Fisher House Foundation for military families.

The center will operate as a part of Naval Hospital Camp Pendleton to treat active-duty military patients who suffer from the physical and psychological effects of brain injury. The center will also provide education and other resources on brain injury for veterans and the wider community.

The center will expand the hospital’s existing program at the Concussion Care Clinic, which has served more than 2,000 patients since 2014. An estimated 550-600 new patients are expected to be referred to the center each year.

“The facility will offer interdisciplinary, state-of-the-art evaluation of service members using clinical, laboratory and imaging resources to guide treatment,” said Cmdr. Paul Sargent, medical director of the Intrepid Spirit center, Naval Hospital Camp Pendleton.

The center’s specialty rehabilitation and therapy programs will focus on providing service members strategies to improve recovery from physical, emotional and spiritual injuries.

“We know that being able to be close to home, surrounded by loved ones, is a crucial part of the recovery process, so we are opening centers on the West Coast this spring at Camp Pendleton and also at Joint Base Lewis-McChord in Washington in order that service members who need treatment do not have to uproot themselves and their families to get it,” said David Winters, president of the Intrepid Fallen Heroes Fund.

Two teams of clinicians will serve the clinic. Their specialties range from neurology, physical medicine and rehabilitation, psychiatry, trauma psychology, neuropsychology and pain psychology to physical and occupational therapy, creative arts therapy and neuro-optometry.

“Our approach is a broadly collaborative center for preventing, treating and researching head trauma and injury to the brain,” Sargent said.

The Intrepid Spirit center includes research, education and clinical staff from the Defense and Veterans Brain Injury Center, which is part of the Department of Defense’s Health Agency.

“Teaching Marines, sailors and their commands about the risks of head injury, how to mitigate concussions and how to understand Traumatic Brain Injury signs and symptoms, along with how to improve readiness is a major goal of our TBI training,” said Regional Education Coordinator Clint Pearman, a certified brain injury specialist with the Defense and Veterans Brain Injury Center.

Pearman provides outreach, education, training and resources for medical personnel, military commands, service members, veterans and family members and civilian community groups from the Camp Pendleton area up to northern California.

The center’s design is based on the original National Intrepid Center of Excellence, which opened in 2010 at the Walter Reed National Military Medical Center in Bethesda, Md., operated by the Department of Defense.

“There are hundreds of thousands of U.S. service members who continue to suffer from traumatic brian injury and other psychological health conditions,” Winters said. “The Intrepid Fallen Heroes Fund has tried to help these brave men and women get the best care available, so we made it our mission to build nine Intrepid Spirit centers that provide comprehensive, state-of-the-art treatment.”

The clinic’s ground breaking was last May and a grand opening ceremony will be held at 11 a.m. April 4 at the Intrepid Spirit Center.

For information about base access, visit pendleton.marines.mil/About/Base-Information/Base-Access.

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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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