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Archive for the ‘NewsBits’ Category

SPEAK OUT! NewsBit . . . . . . NFL Rookie Retires

NFL Rookie Retires
(This news underscores the previous NewsBit.)

presented

by

Donna O’Donnell Figurski

 

johnson_combine Clemson Safety Jadar Johnson was undrafted in the 2017 draft. As a Free Agent, though, he was signed by the New York Giants of the NFL (National Football League). Many thought he was a diamond-in-the-rough. DiamondJadar himself was excited and said he would do “whatever” it takes to become part of the team that the Giants field on Sundays. But, before he played a single regular-season game, he abruptly retired. His agent’s statement said “… and he values his health. …” Some say that Jadar retired because he became aware of the research on NFL brains recently published in the CTEJournal of the American Medical Association. That article showed that 99% of autopsied NFL brains (110/111) had the devastating and contact-sport-specific brain disease CTE (chronic traumatic encephalopathy).

 

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SPEAK OUT! News Bit . . . . . Football, Brain Injury & Kids

Football, Brain Injury & Kids

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by

Donna O’Donnell Figurski

 

newsboy-thIs American football a dying sport? With football’s prominence in American culture, it seems safe to assume no one would predict that its days are numbered. But, there is a growing undercurrent that may eventually lead to the demise of football as we know it. There is more and more evidence that the constant subconcussive hits experienced by football players lead to a high risk of the brain disease CTE (chronic traumatic encephalopathy). CTE can lead to early dementia, football12depression, suicidal thoughts, or problems with cognition, memory, or impulsive behavior.

Recently published by the Journal of the American Medical Association is more evidence of the enormous risk of developing CTE by playing American football. (CTE can at present only be confirmed upon studying brain tissue at autopsy, although research is being directed to finding a test that can detect CTE in the brains of living players.) A study of 202 brains of former football players was done by researchers at the VA Boston Healthcare System and Boston University. They found CTE in 87% of all the brains studied. Of the 110 brains of former professional players in the NFL (National Football League, the premier professional football league in the US), 109 (99%) showed CTE. Playing only college football did not significantly reduce the risk of having CTE, which was found in 91% of the brains of former college players. Playing less football did seem to lower the risk. Only 27% of the brains of former players who played through high school, but no further, showed evidence of CTE. Also, the severity of CTE was probably less with less playing time.

brain4The results have important implications for players. Many players feel they’ve been left ignorant of the risks of brain injury by the NFL, or worse, assured by the league that there is minimal risk. [Some players have quit or retired early (1, 2). Recently, a class-action lawsuit about concussions brought by former players against the NFL was settled for $1 billion.] The NFL has argued, and most players and fans who know about CTE believe, that the brains being studied are biased toward CTE because the autopsied brains in large part are from players already suspected of having a brain injury. Dr. Ann McKee, a Boston University researcher who has examined many of the brains, has stated that the results are staggering even for a biased sample (go to 1:35:58 in the video). She has stated, “It is no longer debatable whether or not there is a problem in football; there is a problem.”

Evidence of any CTE in high school football players is particularly disturbing (go to 1:29:08 in the video). Parents have taken note. Even though the NFL is actively promoting football directly to children, enrollment in youth football leagues is significantly down. Dr. Bennet Omalu, who discovered CTE by studying the brain of Mike Webster, the football-teamfamous Pittsburgh Steeler Center, wrote an Op-Ed in the New York Times titled “Don’t Let Kids Play Football.” During my radio interview of George Visger, a former lineman for the NFL’s San Francisco 49ers who had to quit the game because of a brain injury, he speculated that the preeminence of football in American society will disappear because the NFL’s talent pool will dry up. He speculates that the cost of liability insurance will be too high for youth football leagues to pay (go to 30 minutes into my interview of him).

There is no doubt that American football is exciting to watch, and there are many benefits to playing such a demanding team sport. But, difficult as it is to believe, it seems likely that the high risk of brain injury will eventually end the game.

 

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SPEAK OUT! NewsBit . . . . . . Repair of Brain Injury in Mice by Transplanted Neurons

Repair of Brain Injury in Mice by Transplanted Neurons

presented

by

Donna O’Donnell Figurski

Newsboy thThis is an incredible finding with strong clinical implications! There already is evidence that transplanted neurons can survive and grow in the brain. The newly introduced neurons can form synapses, and they sometimes improve function by partially compensating for a damaged brain circuit. What was not known was whether the original damage could be repaired. Now scientists have shown in a well-studied mouse model of the brain that transplanted neurons can replace the damaged neurons, make the appropriate connections, and repair the damage.ridkk855t

The research was done in Germany by scientists at the Ludwig-Maximilians University Munich in Planegg, the Max Planck Institute of Neurobiology in Martinsried, the Helmholtz Center Munich, and the German Research Center for Environmental Health in Neuherberg. Neurons in the visual cortex of the adult mouse brain were killed, then immature (embryonic) mouse neurons from the cerebral cortex were transplanted into the damaged area of the adult mouse brain. What the scientists found was remarkable. The transplanted neurons developed into mature cells – the same kind as the killed cells, and the new cells replaced the killed cells to give normal function. The process took several months.th-1

The visual cortex is one of the best studied areas of the mouse brain. The structures and connections of the nerve cells are known. So, the scientists, using sophisticated tools, were able to propose that the transplanted neurons used the same developmental signals that were used by the original cells. The transplanted immature neurons developed the proper structures, targeted the same areas of the brain, and made the same connections throughout the brain as did the original cells. The transplanted cells repaired the damaged circuits and allowed the visual cortex to function normally again.gray-mouse-hi-1

This basic research in mice has astonishing clinical implications for humans. (I wrote before about how the mouse is a good first model for the human.) Lost or damaged neurons can be replaced with incredible precision. That means there may be a future treatment, maybe even a cure, for all kinds of damage to the brain, including that which occurs from acquired and traumatic brain injuries, stroke, and neurodegenerative diseases, like Parkinson’s Disease and Alzheimer’s Disease. (Full story)

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SPEAK OUT! NewsBit . . . . . . Repair of Neural Circuits in Stroke-damaged Mouse Brains

SPEAK OUT! NewsBit

Repair of Neural Circuits in Stroke-damaged Mouse Brains

presented by

Donna O’Donnell Figurski

 

 

newsboy-thBasic research on the repair of damaged mouse brains has again produced a potential breakthrough for human therapy. The research may accelerate our ability to repair damaged human brains. A trial study for using this therapy in humans is now being designed.

I’ve already written about the extraordinary promise of cell therapy in eliminating or greatly reducing the effects of brain damage. Much of this promise has to do with the discovery of stem cells, which have the stunning ability to develop into virtually any kind of cell. (The previous NewsBit, however, showed that scientists found a way to cause a common cell type to develop into functional neurons directly without going through a stem-cell stage.) In a study earlier this year, scientists showed that stem cells surgically implanted into damaged human brains reduced the severity of symptoms. But in that study, the scientists were surprised to find that the added stem cells themselves did not become new neurons and form new circuits, but they somehow revved up the brain’s natural ability to heal itself.animal-cell-hi

Now scientists at the University of Southern California (USC) with help from scientists at the National Institutes of Health (NIH) have found a way to activate the implanted stem cells so they develop into neurons and become part of new neural circuits. The direct involvement of the added stem cells resulted in enhanced repair and a much greater loss of symptoms. One NIH scientist said, “If the therapy works in humans, it could markedly accelerate the recovery of these patients.”

CellScientists had previously shown that an FDA (Food and Drug Administration)-approved reagent, the engineered protein 3K3A-APC, caused stem cells in culture to become neurons. The USC scientists wanted to see if 3K3A-APC would help the recovery of a brain-injured animal. The model used for brain damage was mice that were induced to have a stroke. The scientists implanted human stem cells and then treated the mice with 3K3A-APC or a placebo (mock-3K3A-APC). Mice that were treated with stem cells + 3K3A-APC did markedly better (some were almost normal) in tests of sensory perception and motor skills than did mice that were treated with stem cells + the placebo. Unlike the earlier study in which the added stem cells did not become neurons, these stem cells did become neurons if the mouse had been treated with 3K3A-APC.

ScientistThe human stem cells not only became neurons, but they also formed normal connections with mouse neurons. Because the implanted cells were human, the scientists were able to use a human-specific toxin to kill only the implanted cells (the mouse cells were resistant to the toxin). When scientists killed the new neurons, the mice lost the signs of recovery. The scientists concluded that 3K3A-APC caused the cells to develop into neurons that then formed functional neural circuits, ultimately leading to recovery.Brain Cell

USC physician-scientist Berislav Zlokovic, M.D., Ph.D., who directed the research, said, “When you give these mice 3K3A-APC, it works much better than stem cells alone. We showed that 3K3A-APC helps the cells convert into neurons and make structural and functional connections with the host’s nervous system.” (Full story)

 

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SPEAK OUT! NewsBit . . . . . . Common Mouse Cell Type Converted to Neurons

SPEAK OUT! NewsBit

Common Mouse Cell Type Converted to Neurons

presented by

Donna O’Donnell Figurski

 

newsboy-thCommon Mouse Cell Type Converted to Neurons

You’ve probably heard of the promising future of cell therapy. The excitement comes from the fact that injuries might be treated by implanting fresh, healthy cells. Stem cells, which can mature to many different cell types, have been discovered in almost every organ in the body. They hold enormous potential for helping to heal injured organs. Already, scientists are devising methods to add new muscle to damaged hearts and to add insulin-producing cells to the body to cure Type I diabetes. The brain also has stem cells, and much of the natural recovery from brain injury is due to stem cells, which rebuild the damaged part of the brain. The beauty of stem cells from the brain is that they can develop into healthy neurons and replace damaged circuits. But the natural healing of the brain is often insufficient. Scientists have been looking for ways to make more stem cells and to activate them so that implanting them is practical and they can result in more healing.scientist

I want to tell you about exciting basic research on cell therapy that may make possible or speed up the development of new therapies for brain injury. Scientists at Duke University have found a way to make neurons from common mouse cells, called “fibroblasts,” without resorting to stem cells. The scientists made a modified protein and put it into fibroblasts. The modified protein found and activated the master regulator genes needed to turn on the genes for the cell to become a neuron.

In the past, a cell’s change into a neuron required that extra copies of the master regulator genes be introduced into the cell. The cell maintained its neuron-like properties only if the extra activators were present. If the extra copies were lost, the cell reverted to its original form. Scientists said that the neurons were “unstable.” Still, it was a breakthrough. To help stabilize the neurons, extra copies of genes for the master regulators were added to its chromosomes. The neurons still weren’t perfectly stable, and the presence of extra copies in the chromosomes was unnatural.

In the new method, activation of the neuron genes is natural. The neurons are “stable,” even when the modified activator protein is gone. As far as the scientists can tell, the neurons formed this way appear to be like natural neurons.

MouseOf course, these studies need to be done with human cells. But, because the mouse is similar enough to humans genetically, new neurons are likely to be made from human cells. If so, cell therapy to treat brain injury will become common in the foreseeable future. One benefit is that therapy can be personalized. It’s not practical to get your neurons from a brain biopsy, but your easy-to-get fibroblasts can be converted to neurons. Those neurons can then be tested with therapeutic drugs to see what works best with your genetic background. Also, the implanted cells would not be rejected by your body (prevention of rejection is the reason for immunosuppressive drugs today) because the neurons would be made from cells of your own body. (Full story)

 

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SPEAK OUT! NewsBit . . . . . . Inosine Helps Brain-Injured Monkeys Recover Fine Motor Control

SPEAK OUT! NewsBit

Inosine Helps Brain-Injured Monkeys Recover Fine Motor Control

presented by

Donna O’Donnell Figurski

My husband, David, is a traumatic brain injury survivor since 2005. He is physically disabled as a result of his brain injury. As a molecular biologist from Columbia University, David is always searching for ways to improve his own life after his brain injury. He recently stumbled on this exciting research project, and we wanted to share this hopeful concept with others.

 

Disclaimer:

Neither David nor I is a medical doctor, and we are not suggesting any medical solutions. We are only publishing this article for your information.

 

Newsboy th

 

Inosine is a small molecule found in cells. Research with mice and rats has shown that inosine is released by stressed or damaged neurons. Inosine can turn on the genes for axon development. Axons are the long, threadlike membrane extensions needed for neurons to send an electrochemical message to other neurons. The new axons from undamaged neurons can rewire the brain (plasticity) to allow circuits to form that compensate for circuits lost from damage.

Adding inosine to neurons in culture stimulates the formation of more axons. Would inosine stimulate an increase in plasticity by increasing axon formation and thereby help recovery from brain injury? Consistent with this idea, neuroscientists found that rats recovered from brain injury better when inosine was present.pTqKnRpgc

Now neuroscientists at Boston University report testing inosine’s effect on a primate – the rhesus monkey. The study was small (8 monkeys) because monkey experiments are expensive, but, despite the small number, the results were significant. At the beginning, all 8 monkeys could easily grasp food treats with their dominant hand. The part of the brain needed for the required motor skills in the dominant hand was then deliberately damaged in each monkey. The 8 brain-injured monkeys were divided into two groups: 4 monkeys were treated by giving them inosine, and 4 were given a placebo. The researchers didn’t know which monkeys were getting inosine and which were getting the placebo.

After 14 weeks of treatment, the monkeys were examined for their ability to grasp a food treat. Three of the four inosine-treated monkeys grasped the food with their dominant hand normally. Fine motor control in the hand seemed to be the way it was prior to the brain injury. In contrast, the placebo-treated monkeys retrieved their food by using a compensatory strategy. The placebo-treated monkeys still had a problem with fine motor control in the hand.

mouse-hiThis preliminary study has extended evidence of the inosine benefit from mice and rats to a primate. The result indicates that inosine may one day benefit human victims of brain injury. Inosine is already in clinical trials for the treatment of multiple sclerosis and Parkinson’s Disease. Inosine appears to be safe – athletes have taken inosine supplements for decades.

Strictly speaking, this experiment addressed recovery of only a specific movement. The brain injuries were highly controlled – all were nearly identical, and they were in a specific area of the frontal lobe that affects fine motor control of the hand. Inosine experiments of this type have only been done in animal models. But even with all these caveats, there is reason to be optimistic. Inosine treatment may become a common human therapy for brain injury. Clearly more research is needed before inosine is shown to be useful in the clinic. (Full story)

 

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SPEAK OUT! NewsBit: . . . . . . Wanting A “Sound Mind,” 30-Year-Old Football Player Retires

Wanting A “Sound Mind,” 30-Year-Old Football Player Retires

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by

Donna O’Donnell Figurski

 

husain_abdullah

Husain Abdullah – NFL Player

For seven years, Husain Abdullah played football in the National Football League (NFL), the premier professional football league in the United States. For four years, Abdullah, a safety, played with the Minnesota Vikings, and, for three years, he played with the Kansas City Chiefs. He graciously thanked both teams for allowing him to play. In the 2015 season, he had the fifth concussion of his career. While he was recovering, he thought about his many life-goals. Husain realized that he would need a “sound mind” to achieve his goals.

The research showing a link between the head trauma of football and the neurodegenerative disease CTE (chronic traumatic encephalopathy) is thought-provoking, and it has several players concerned. Even the NFL has admitted that there is a link between playing football and CTE, although the league later tried to downplay its comment. (CTE, originally known as “dementia pugilistica,” had only been seen in the brains of some boxers.

Dr. Bennet Omalu -

Dr. Bennet Omalu –

Dr. Bennet Omalu was the first to find the disease elsewhere – in a football player. Dr. Omalu renamed the disease “CTE.” Dr. Omalu’s discovery is the subject of the December 2015 movie Concussion, starring Will Smith. The real-life story is told in the PBS Frontline documentary, League of Denial: The NFL’s Concussion Crisis – available free online.)

Abdullah’s retirement follows other early retirements, most notably that of San Francisco 49er star rookie linebacker, Chris Borland, who cited the high risk of brain disease as his reason for retiring after playing only one year. Another rookie, Green Bay Packer wide receiver Adrian Coxson, retired after getting a severe concussion in practice and being told that the next hit might seriously affect his brain function or kill him.

Abdullah Husain - NFL Player

Abdullah Husain – NFL Player

It remains to be seen if Husain Abdullah’s retirement will be the last early retirement in the NFL due to football’s risk to the brain. (Full story)

 

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No memory of the day that changed my life

My name is Michelle Munt and this is my story about surviving a brain injury and what I continue to learn about it. This is for other survivors and their loved ones, but also to raise awareness of what can happen to those in an accident. This invisible injury too often goes undiagnosed and it can be difficult to find information about it. I will talk about things that have helped me as I continue to recover and invite others to see if it works for them too.

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