Neuroscience Advances Archives - Amazing Health Advances

Antibiotics Destroy Memories?

The AHA! Team — Thu, 05 Dec 2024 06:09:34 +0000

Al Sears, MD, CNS – A study by epidemiologists at Harvard Medical School reveals a crucial link between your gut’s reaction to antibiotics – especially when taken during midlife and older – and a dramatic decline in cognitive ability as you age. Even in my earliest days of practicing medicine, I was never a big fan of prescribing antibiotics – except, of course, in cases of extreme or life-threatening infections. Because even back then, I was concerned about the damage these drugs could cause to your gut. That’s because trillions of microscopic bacteria – some that protect against certain diseases and some that can cause disease – live in your microbiome and exist in a delicate balance with each other. The problem is that antibiotics can’t distinguish between so-called “good” bacteria and the “bad” ones causing the infection. These drugs kill everything they touch. You see, this microbiome of bacteria and other microbes is essential to almost every aspect of your health – from your immune system and how much energy you have to the absorption of nutrients and even your vulnerability to depression. Now a study by epidemiologists at Harvard Medical School reveals a crucial link between your gut’s reaction to antibiotics – especially when taken during midlife and older – and a dramatic decline in cognitive ability as you age. This makes sense because your gut microflora acts like a biochemical telegraph system that sends messages along your vagus nerve directly to your brain. Don’t get me wrong. I’m not against antibiotics, per se. Since the rollout of penicillin in the 1940s, and the other antibiotics that followed, these drugs have saved hundreds of millions of lives in the fight against diseases like tuberculosis, pneumonia, and diphtheria. I am against their overuse. And now there’s one more reason to stop overusing these drugs… Studying the data of more than 14,000 women from the Nurses’ Health Study project, Harvard scientists found that taking antibiotics for two months or more during midlife was “significantly” linked to poorer cognition, learning, and memory scores , as well as reduced psychomotor speed and attention.1 The researchers noted that the decline in brain power was the equivalent of losing about three or four years of normal aging. The message of the study is loud and clear – keep your antibiotic use to a bare minimum. There are still too many doctors who hand these dangerous drugs out like candies whenever a patient appears with a sore throat, cough, or a urinary tract infection. According to the Centers for Disease Control and Prevention, around 1 in 3 antibiotic prescriptions are unnecessary.2 But the problem isn’t just confined to prescription antibiotics. Antibiotics are pumped into industrialized cattle and poultry to fight bacterial infections that spread through cramped feedlots and battery chicken farms. They are also sprayed onto fruit trees and industrial vegetable farms to prevent and treat infection. During spraying, the wind can carry them further afield into the water supply. 3 Simple Steps To Protect Yourself From Antibiotics Protecting yourself from the damage of antibiotics requires a three-pronged strategy… Avoid Cheap Meats: Cattle and poultry pumped full of antibiotics are now awash in our food supply. Make sure the meat you purchase is always grass-fed, pastured, and antibiotic free. Unless you know the source of the meat and the practices of the ranch or farm, the safest foods are USDA-certified organic foods. If your grocer doesn’t carry them, let them know you’ll shop elsewhere. Bulk up Your Immune System: A strong immune system is essential, not just for fighting infections – but also for fighting the effects of antibiotic use. Two of my favorite immune system boosters are: Anamu. Studies show this South American herb contains a powerful compound called dibenzyl trisulphide, which is a potent stimulator of your body’s “T helper cells.” Their job is to give other immune cells an extra boost.3 Anamu capsules are available at most health food stores. I suggest taking 500 to 1,000 mg per day in divided doses. Astragalus. This herb has been used in Traditional Chinese Medicine for millennia to strengthen the body’s immune defenses. Astragalus is called an “adaptogen,” meaning it helps protect the body against physical and mental stresses. I recommend 500 mg of the concentrated extract three times a day. Replace Big Pharma Meds with Natural Antibiotics: Nature has given us hundreds, if not thousands, of herbal alternatives. A few good ones are: Garlic. Research has found that garlic can be an effective treatment against many forms of bacteria, including Salmonella and E. coli. Garlic has also been shown to be effective against drug-resistant tuberculosis bacteria. Honey. Multiple studies reveal honey to be a powerhouse natural antibiotic, with the ability to inhibit more than 60 kinds of bad bacteria.4 The best is raw honey and always avoid pasteurized honey products. Curcumin. This is the main ingredient in the spice turmeric, and it’s one of the cornerstones of ancient Ayurvedic medicine. Thousands of studies prove curcumin beats a long list of modern drugs, including antibiotics. A recent study found curcumin killed 100% of the MRSA superbug within 2 hours.5 To Your Good Health, Al Sears, MD, CNS References: 1. Mehta RS, et al. “Association of midlife antibiotic use with subsequent cognitive function in women.” March 2022. Plos One. 17(3):e0264649. 2. “1 in 3 antibiotic prescriptions unnecessary: New CDC data show large percentage of antibiotics misused in outpatient settings.” CDC. May 3, 2016. Available at: https://www.cdc.gov/media/releases/2016/p0503-unnecessary-prescriptions.html 3. Williams LA, et al. “A critical review of the therapeutic potential of dibenzyl trisulphide isolated from Petiveria alliacea L (guinea hen weed, anamu).” West Indian Med J. 2007 Jan;56(1):17-21. 4. Mandal MD, Mandal S. “Honey: its medicinal property and antibacterial activity.” Asian Pac J Trop Biomed. 2011 Apr;1(2):154-60. 5. Poonam Tyagi, et al. Bactericidal Activity of Curcumin I Is Associated with Damaging of Bacterial Membrane. PLoS One. 2015;10(3):e0121313. To read the original article click here.

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Promising New Drug Could Slow Progression of ALS

The AHA! Team — Mon, 25 Nov 2024 06:46:21 +0000

John Jeffay via Israel21c – A chance encounter with an inspiring ALS patient, prompted Alon Ben-Noon to set up NeuroSense Therapeutics, a startup developing a drug combo that aims to slow progression of ALS and other neurodegenerative diseases. It was a life-changing moment for Alon Ben-Noon when he first met Shay Rishoni. Rishoni, once a keen runner and cyclist, had been robbed of all movement by the devastating and degenerative disease ALS. It was 2016 and Rishoni was by then immobile, only able to communicate by staring at an eye-tracking computer screen. But that didn’t stop him working as CEO of Prize4Life, a nonprofit founded by other ALS patients to help find a treatment for the disease. Ben-Noon was profoundly moved by the meeting. “I looked at myself and I thought: You’re completely functioning, but you’re not doing half of what he’s doing. He’s completely paralyzed and he’s moving mountains.” Ben-Noon was already working in the pharmaceutical industry, as a consultant, but decided to change track and do everything he could to allow ALS patients to live longer and live better. And so NeuroSense Therapeutics was born. The pharmaceutical startup, based in Herzliya, central Israel, aims to slow the progress of ALS (amyotrophic lateral sclerosis) as well as Alzheimer’s and Parkinson’s, which are also neurodegenerative disorders. PrimeC ALS is a rare and incurable disease caused by the death of motor neurons, the nerve cells that send messages from the brain and spinal cord to our muscles and glands. ALS (also known as Lou Gehrig’s disease) leads to complete paralysis, followed by death, usually with two to five years. Rishoni, married with two sons, was diagnosed when he was 45 and survived another seven years, which is longer than most. At the time, the only medication available was a drug called Riluzole, approved for use in 1995, which extended patients’ lives by around three months. Ben-Noon was determined to do better. He gathered a team of experts to identify molecules in existing drugs that could be combined to attack multiple targets associated with ALS. Previous attempts to treat the disease had focused on single targets. The team succeeded in addressing a number of distinct problems, including the degeneration of motor neurons. In clinical trials in Israel, Canada and Italy, the drug that NeuroSense developed has been shown to give ALS patients, on average, an extra 18 months. Patients experienced a 36% slower disease progression and a 43% better survival rate over 12 months compared to control subjects. The drug is named PrimeC – “prime” is English for “Rishoni” — and could be available for patients within three and a half years. The patented drug combines the antibiotic ciprofloxacin and the anti-inflammatory agent celecoxib, both already approved by the US Food and Drug Administration (FDA) for unrelated conditions. Fast progression ALS is a highly aggressive and complex disease that affects around one in 10,000 people. Initial symptoms are mild, such a weakness in a finger, or dragging a leg, but it can progress at an alarming rate. “Quality of life in terms of functionality is usually quite good at the beginning and then it declines as the disease progresses,” says Ben-Noon. “One day a patient can still eat by himself; the next day they’ll need assistance. One day a patient can walk independently and the next day they’ll have difficulties walking without a cane and soon they’ll need a wheelchair. “We understood quite quickly that we cannot reverse the disease, but we can stop it and make a meaningful change to people’s lives.” But he hopes to do even more. “Eventually, we will create a world where ALS is a non-fatal disease. Patients will live life to the full, happily, maybe with a very small dysfunction. That’s it, that’s the vision,” Ben-Noon says. Orphan drug designation NeuroSense has received orphan drug designation in the US and Europe, recognizing its potential to treat a rare condition (which means tax breaks and other benefits for the company) though it still needs to gain regulatory approval pending further clinical trials. The company, which went public on NASDAQ in December 2021, has so far attracted $30 million in funding and has a US office in Cambridge, Massachusetts. “We are only 16 employees but we work with dozens of consultants and vendors who are assisting us in advancing our programs,” says Ben-Noon. Dr. Vivian Drory, director of the ALS clinic at Tel Aviv Sourasky Medical Center, said that promising results from the company’s 12-month clinical study highlight the significant potential of PrimeC as a disease-modifying drug for ALS. “These findings underscore the importance of early intervention, which can lead to more substantial benefits, and provide valuable insights that will inform the design of the company’s Phase 3 study, increasing the likelihood of success,” she said. It’s often small companies, like NeuroSense, that pioneer new drugs, Ben-Noon notes. “Nowadays the ratio is about 60/40 — 60 for the small companies 40 for big pharma,” says Ben-Noon. “In many cases it starts in a very small company like ours and then a big pharma looks at the outcomes and decides to buy out the company and continue the development.” Looking back to his first meeting with Rishoni, back in 2016, does he feel he’s done what he set out to achieve? “Yes, absolutely,” he says. “We always keep in touch with Tami [Rishoni’s widow]. We talk, we meet and every time we reach a new milestone is very fulfilling.” “If I hadn’t bumped into Shay,” he reflects, “I probably would still be doing medical consulting work. But now I’m very proud to say we’re creating change in the world.” For more information, click here. To read the original article click here.

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Engineered ‘Cat Parasite’ Helps Deliver Drugs to Brain

The AHA! Team — Fri, 01 Nov 2024 05:35:21 +0000

Yulia Karra via Israel21c – Researchers discover method to penetrate the blood-brain barrier and deliver therapeutic proteins via Toxoplasma gondii. Researchers from Tel Aviv University (TAU) recently discovered a method to deliver neurological treatment to the human brain using an engineered version of Toxoplasma gondii, commonly known as “the cat parasite.” One of the biggest challenges in treating neurological diseases is getting the therapeutic drugs through the blood-brain barrier (BBB). “It is very difficult to deliver drugs to the brain via the bloodstream; this is especially true for large molecules such as proteins, the critical ‘machines’ that carry out many important functions inside the cell,” said Prof. Oded Rechavi from TAU’s Department of Neurobiology and Sagol School of Neuroscience, who led the study. The study was conducted in collaboration with Rechavi’s PhD student Shahar Bracha, and Prof. Lilach Sheiner, an Israeli scientist and toxoplasma expert from The University of Glasgow. The findings were recently published in the scientific journal Nature Microbiology. Cat parasite To solve the BBB problem, the research team utilized Toxoplasma gondii, which can infect a vast variety of organisms, including humans, but reproduces only in the guts of cats. It is estimated that a third of the global population is infected by the parasite at some point in their lives. “Most people don’t even feel the infection or only experience mild flu-like symptoms,” added Rechavi. What made the parasite the perfect candidate for the novel study is its ability to penetrate the human brain and survive there in a dormant state, without reproducing. This prompted the team to genetically engineer Toxoplasma gondii to secrete therapeutic proteins. “The parasite has three distinct secretion systems,” explained Rechavi. “One of the systems ‘shoots’ a ‘harpoon’ into the neuron, to enable penetration. Once inside, the parasite forms a kind of cyst in which it continues to secrete proteins permanently. We engineered the parasite’s DNA to make it produce and secrete the proteins we want, which have therapeutic potential.” The methodology As part of the study, the team injected transgenic model animals with the genetically engineered parasite to produce and secrete proteins that travel into cell nuclei. Transgenic animals normally have a foreign gene deliberately inserted into their genome. The scientists then gathered enough evidence to prove that the proteins had been delivered to the target area and remained active in the neurons’ nuclei. The current study focused primarily on a protein called MeCP2, whose deficiency is associated with Rett syndrome, a rare neurological disorder that affects the way the brain develops. Researchers emphasized, however, that the method could prove useful in the treatment of a series of diseases caused by deficiency or abnormal expression of a certain protein. To ensure the method’s safe and effective therapeutic implementation, for both drug delivery and genetic editing, a company named Epeius Pharma, was established in collaboration with Ramot, the technology transfer company of Tel Aviv University, and with the University of Glasgow’s research and innovation services. To read the original article click here.

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Brain Cell Grafts in Monkeys Jump-Start Human Trial for New Parkinson’s Treatment

The AHA! Team — Mon, 28 Oct 2024 05:21:55 +0000

University of Wisconsin–Madison via Newswise – People with Parkinson’s disease are receiving a new treatment in a clinical trial started after University of Wisconsin–Madison scientists demonstrated the safety and feasibility of the therapeutic delivery method in a study of non-human primates. People with Parkinson’s disease are receiving a new treatment in a clinical trial started after University of Wisconsin–Madison scientists demonstrated the safety and feasibility of the therapeutic delivery method in a study of non-human primates. Parkinson’s disease damages neurons in the brain that produce dopamine, a brain chemical that transmits signals between nerve cells. The disrupted signals make it progressively harder to coordinate even simple movements and cause rigidity, slowness and tremors that are the disease’s hallmark symptoms. Patients are typically treated with drugs like L-DOPA to increase dopamine production. Although the drugs help many patients, they present complications and lose their effectiveness over time. Parkinson’s disease damages neurons in the brain that produce dopamine Researchers at the Wisconsin National Primate Research Center successfully grafted brain cells called dopaminergic neuronal progenitor cells into the brains of cynomolgus macaque monkeys. California-based Aspen Neuroscience provided the cells, grown from multiple lines of human induced pluripotent stem cells, along with key pieces of the equipment for delivering them to specific parts of the brain. “By the time of diagnosis, it is common for people with Parkinson’s to have lost the majority of dopaminergic neurons, leading to progressive loss of motor and neurological function,” explains Edward Wirth III, an expert in cell therapies, study co-author and Aspen’s chief medical officer. “To replace these lost cells, we must target a very specific area of the brain with a high degree of surgical precision. Utilizing the latest advances in intraoperative MRI guided techniques, the patient’s new cells are transplanted, a few microliters at a time, to the exact area where they are most needed.” Working with potential cell therapies in pursuing treatments for Parkinson’s disease is a particular specialty of the team at Marina Emborg’s lab and their primate center colleagues. “Using autologous cells, a patient’s own cells, avoids the need to use immunosuppression to keep the patient’s body from rejecting or attacking the graft,” says Emborg, a UW–Madison professor of medical physics. “Aspen has developed the technological methods for manufacturing, for quality control, that makes it feasible at scale to make autologous cells and get them to the patients.” The researchers’ results in non-human primates, which supported Aspen’s successful Investigational New Drug application to the Food and Drug Administration to begin human trials, were published today in the Journal of Neurosurgery. “This study was an important step in our work to bring the promise of a cell-replacement therapy to people with Parkinson’s disease” “This study was an important step in our work to bring the promise of a cell-replacement therapy to people with Parkinson’s disease,” says Andrés Bratt-Leal, study co-author, Aspen Neuroscience co-founder and senior vice-president of research and development. “The results were instrumental in opening our first-in-human trial and informing how we deliver patients’ own cells to them in the study.” The UW–Madison scientists, led by Parkinson’s researcher Emborg, took up the Aspen-funded work fresh off their own success (published in 2021) reversing Parkinson’s symptoms in monkeys by grafting neurons grown from the monkeys’ own cells, called an autologous transplant. The 2021 study, using cells grown by UW–Madison stem cell researcher Su-Chun Zhang, added new dopamine-producing neurons to each animal’s brain through injections guided in real time by MRI to an area of the brain called the putamen. Dopamine production increased dramatically, as did the monkeys’ motor skills. At the same time, symptoms of depression and anxiety were reduced. The new study was designed to test the delivery of Aspen’s human cells. Wirth and Aspen scientists worked with Emborg’s team to bridge the monkey-to-human application. While Emborg’s previous study administered cells to the putamen through the top of the skull, the Aspen study examined cell administration through the back of the skull — an angle that could allow surgeons to reach their target with fewer insertions of the apparatus that delivers the new cells into the brain. “The core idea is to decrease the risk of infection, the trauma, the surgical time the patient spends under anesthesia,” Emborg says. “The fewer tracks you have to follow through the brain, the better for all of that.” Six monkeys received grafts of the human neurons Six monkeys received grafts of the human neurons through two paths in each side, or hemisphere, of their brains, with more cells deposited on one side of the brain than the other. A control group of three animals underwent the procedure without the cell delivery. “In tissue samples taken seven and 30 days after the procedures, we found the grafted cells persisted in five of the animals,” Emborg says. The researchers confirmed the presence of Aspen’s human neurons in the monkeys’ brains, finding more cells in the hemispheres that were injected with a higher dose, more cells in the 30-day tissue samples compared to the seven-day samples and the presence of a protein produced by young neurons working to integrate with neighboring cells — all signs the cells grafts were successful. It was a true collaboration, according to Emborg — between the Aspen scientists, her lab and the Wisconsin National Primate Research Center veterinarians and staff — to validate the company’s procedures and equipment before study co-author Paul Larson, a neurosurgeon at Banner – University Medical Center Tucson and professor of neurosurgery at the University of Arizona College of Medicine – Tucson, began Aspen’s first-in-human trial with people with Parkinson’s in April. The work done to refine the logistics, surgical equipment and techniques in the animal procedures will inform the way patients in the human trial receive and recover from the new therapy, providing hope for those struggling with a debilitating disease. “Our results were all so exciting,” Emborg says. “And then, when I saw they had been able to begin with a human patient this spring, I just had tears in my eyes.” To read the original article click here.

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Low-Dose Ketamine Eases Fentanyl Withdrawal Symptoms

The AHA! Team — Thu, 17 Oct 2024 08:22:08 +0000

University of Washington School of Medicine via News-Medical – Drug overdose is the leading cause of injury deaths in young adults in the United States, with fentanyl causing over 70,000 deaths annually. Many people who use fentanyl become trapped in their addiction out of fear and a low tolerance for the withdrawal symptoms, which include muscle cramps, nausea, chills, sweats and intense cravings. They can’t stop using fentanyl, and they also have trouble starting either of the two medications, methadone and buprenorphine, that can dramatically reduce their risk of overdose death. Research findings published Aug. 29 in Addiction Science & Clinical Practice may offer hope. A pilot study showed that a small amount of ketamine can reduce or eliminate the withdrawal symptoms associated with quitting fentanyl. “The main takeaway is that we have found an easier way for people trapped in the grip of fentanyl addiction to get started in treatment.” Dr. Lucinda Grande, clinical assistant professor of family medicine, University of Washington School of Medicine She was the study’s lead author. “Methadone can be difficult to access due to strict federal regulations, and starting buprenorphine can cause severe withdrawal symptoms before those who start it become stabilized,” added study co-author Dr. Tom Hutch. He is the medical director of the opioid treatment program at We Care Daily Clinics in Auburn, Wash. “Ketamine, at an imperceptibly low dose, helps bridge that gap.” Over 14 months, Grande and colleagues in Auburn and Olympia prescribed ketamine to 37 fentanyl-addicted patients whose fear of withdrawal symptoms had deterred them from trying buprenorphine. Twenty-four patients actually tried the drug, and 16 completed the transition to buprenorphine. Most patients reported a reduction or elimination of withdrawal symptoms after each ketamine dose, the effect of which lasted for hours. Of the last 12 who completed the transition, 92% remained in treatment for at least 30 days. Patients placed a ketamine lozenge or syrup under the tongue. The 16 mg dose is a small fraction of that typically used for anesthesia, the main clinical role of ketamine for 50 years, according to Grande. That dosage also is less than half of the smallest ketamine dose prescribed for depression treatment, an increasingly common use of this medication. Researchers monitored patients daily or almost daily, and refined the treatment strategy based on patient response and prescriber experience. Grande developed the concept after she learned that emergency-medicine physician and coauthor Dr. Andrew Herring of Oakland, California, used a higher, sedating dose of ketamine successfully in his emergency department to resolve a patient’s severe case of withdrawal from fentanyl addiction. Grande is a primary-care and addiction doctor in practice near Olympia who, in the past dozen years, has used low-dose ketamine to treat more than 600 patients for chronic pain and depression. Ketamine has gained prominence in the news since actor Matthew Perry of the sitcom “Friends” overdosed on the drug and drowned. Perry had undergone high-dose ketamine treatment for depression, news reports have suggested. “Our study underscores the enormous potential of this medication for addressing important health problems such as depression, chronic pain and now fentanyl-use disorder,” said Grande. Ketamine’s positive attributes have been overshadowed by Perry’s death, she said. Grande hopes this pilot study’s results will be confirmed by larger studies. “I am excited about these results,” she said. “This is a wonderful opportunity to save lives.” Source: University of Washington School of Medicine Journal reference: Grande, L., et al. (2024) Ketamine-assisted buprenorphine initiation: a pilot case series. Addiction Science & Clinical Practice. doi.org/10.1186/s13722-024-00494-2. To read the original article click here.

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New Brain-Computer Interface Allows Man with ALS to ‘Speak’ Again

The AHA! Team — Fri, 11 Oct 2024 08:20:41 +0000

UC Davis Health via Newswise – Technology developed by UC Davis Health restores interpersonal communication A new brain-computer interface (BCI) developed at UC Davis Health translates brain signals into speech with up to 97% accuracy — the most accurate system of its kind. The researchers implanted sensors in the brain of a man with severely impaired speech due to amyotrophic lateral sclerosis (ALS). The man was able to communicate his intended speech within minutes of activating the system. A study about this work was published today in the New England Journal of Medicine. ALS, also known as Lou Gehrig’s disease, affects the nerve cells that control movement throughout the body. The disease leads to a gradual loss of the ability to stand, walk and use one’s hands. It can also cause a person to lose control of the muscles used to speak, leading to a loss of understandable speech. The new technology is being developed to restore communication for people who can’t speak due to paralysis or neurological conditions like ALS. It can interpret brain signals when the user tries to speak and turns them into text that is ‘spoken’ aloud by the computer. “Our BCI technology helped a man with paralysis to communicate with friends, families and caregivers,” said UC Davis neurosurgeon David Brandman. “Our paper demonstrates the most accurate speech neuroprosthesis (device) ever reported.” Brandman is the co-principal investigator and co-senior author of this study. He is an assistant professor in the UC Davis Department of Neurological Surgery and co-director of the UC Davis Neuroprosthetics Lab. The new BCI breaks the communication barrier When someone tries to speak, the new BCI device transforms their brain activity into text on a computer screen. The computer can then read the text out loud. To develop the system, the team enrolled Casey Harrell, a 45-year-old man with ALS, in the BrainGate clinical trial. At the time of his enrollment, Harrell had weakness in his arms and legs (tetraparesis). His speech was very hard to understand (dysarthria) and required others to help interpret for him. In July 2023, Brandman implanted the investigational BCI device. He placed four microelectrode arrays into the left precentral gyrus, a brain region responsible for coordinating speech. The arrays are designed to record the brain activity from 256 cortical electrodes. “We’re really detecting their attempt to move their muscles and talk,” explained neuroscientist Sergey Stavisky. Stavisky is an assistant professor in the Department of Neurological Surgery. He is the co-director of the UC Davis Neuroprosthetics Lab and co-principal investigator of the study. “We are recording from the part of the brain that’s trying to send these commands to the muscles. And we are basically listening into that, and we’re translating those patterns of brain activity into a phoneme — like a syllable or the unit of speech — and then the words they’re trying to say.” Faster training, better results Despite recent advances in BCI technology, efforts to enable communication have been slow and prone to errors. This is because the machine-learning programs that interpreted brain signals required a large amount of time and data to perform. “Previous speech BCI systems had frequent word errors. This made it difficult for the user to be understood consistently and was a barrier to communication,” Brandman explained. “Our objective was to develop a system that empowered someone to be understood whenever they wanted to speak.” Harrell used the system in both prompted and spontaneous conversational settings. In both cases, speech decoding happened in real time, with continuous system updates to keep it working accurately. The decoded words were shown on a screen. Amazingly, they were read aloud in a voice that sounded like Harrell’s before he had ALS. The voice was composed using software trained with existing audio samples of his pre-ALS voice. At the first speech data training session, the system took 30 minutes to achieve 99.6% word accuracy with a 50-word vocabulary. “The first time we tried the system, he cried with joy as the words he was trying to say correctly appeared on-screen. We all did,” Stavisky said. In the second session, the size of the potential vocabulary increased to 125,000 words. With just an additional 1.4 hours of training data, the BCI achieved a 90.2% word accuracy with this greatly expanded vocabulary. After continued data collection, the BCI has maintained 97.5% accuracy. “At this point, we can decode what Casey is trying to say correctly about 97% of the time, which is better than many commercially available smartphone applications that try to interpret a person’s voice,” Brandman said. “This technology is transformative because it provides hope for people who want to speak but can’t. I hope that technology like this speech BCI will help future patients speak with their family and friends.” The study reports on 84 data collection sessions over 32 weeks. In total, Harrell used the speech BCI in self-paced conversations for over 248 hours to communicate in person and over video chat. “Not being able to communicate is so frustrating and demoralizing. It is like you are trapped,” Harrell said. “Something like this technology will help people back into life and society.” “It has been immensely rewarding to see Casey regain his ability to speak with his family and friends through this technology,” said the study’s lead author, Nicholas Card. Card is a postdoctoral scholar in the UC Davis Department of Neurological Surgery. “Casey and our other BrainGate participants are truly extraordinary. They deserve tremendous credit for joining these early clinical trials. They do this not because they’re hoping to gain any personal benefit, but to help us develop a system that will restore communication and mobility for other people with paralysis,” said co-author and BrainGate trial sponsor-investigator Leigh Hochberg. Hochberg is a neurologist and neuroscientist at Massachusetts General Hospital, Brown University and the VA Providence Healthcare System. Brandman is the site-responsible principal investigator of the BrainGate2 clinical trial. The trial is enrolling participants. To learn more about the study, visit braingate.org or contact braingate@ucdavis.edu. A complete list of coauthors and funders is available in the article. Caution: Investigational device. Limited by Federal law to investigational use. To read the original article click here.

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Dad’s Quest to Aid Son Leads to Stroke-Recovery Technology

The AHA! Team — Wed, 09 Oct 2024 08:31:39 +0000

John Jeffay via Israel21c – BRAIN.Q helmet’s tailored, low-intensity, low-frequency electromagnetic stimulation aims to enhance and accelerate the brain’s recovery after stroke. Yaron Segal has, like many thousands of enterprising Israelis, identified a problem. And like so many in a country driven by technological innovation, he’s established a startup to find a solution. But he’s not so interested in the payday “exit” that attracts most entrepreneurs in the Startup Nation. His ultimate goal is to find a treatment for his son Lear, born 23 years ago born with familial dysautonomia, a rare and progressive genetic neurological disorder. Segal is not an obvious candidate for the job. He trained as a physicist, specializing in climate, satellites, and three-dimensional models of the atmosphere. But when Lear was diagnosed at the age of three months, Segal decided that he would devote his energy, passion and intellect to finding an effective treatment. Remarkable discoveries He isn’t there yet, but in the long – and often frustrating – process of trying, he has made some remarkable discoveries about the brain’s ability to repair itself, and has developed a treatment that has the potential to help stroke patients live more independent lives. Segal is confident that the same technology will, at some point in the future, also benefit people living with depression, PTSD, ADHD, spinal cord injuries, traumatic brain injuries and other brain-related conditions … and familial dysautonomia. His noninvasive, cloud-based “brainwave helmet” activates a low-intensity electromagnetic field around the patient’s head. In clinical trials with stroke patients, it was demonstrated the treatment significantly improved outcomes in the treated group compared to the control group. It is believed that the investigational technology device encourages the growth of new links between brain cells – links that can get broken by a trauma, or in the case of familial dysautonomia, never existed in the first place. BRAIN.Q, the startup Segal cofounded in 2016, now has 25 staff in Israel and the USA and has attracted $50 million in funding. The crazy guy Segal was, as he puts it, “the crazy guy” who became convinced that the adult brain was capable, with encouragement, of repairing itself. Not completely, but significantly. His theory flew in the face of received medical wisdom. “Neuroplasticity” is the brain’s ability to change and adapt throughout a person’s life and reorganize its structure, functions and connections in response to new experiences, learning or environmental changes. But that couldn’t happen fully in damaged parts of the brain where there is no neural activity – until Segal’s breakthrough. He started experimenting in 2010, funded by friends and family, and within two years he’d shown that mice and rats could, with an early form of his treatment, learn to walk and function again after suffering a brain injury or a broken spinal cord. A potential investor showed the raw data from Segal’s experiment to an expert, who simply refused to accept it was possible. The dismissive response, Segal recalls, was: “I don’t believe it happened. You cannot revive links between cells.” Segal was disappointed but not dismayed. The next step was to test his breakthrough on humans. Faster recovery In a clinical trial conducted in India, stroke patients received the BRAIN.Q therapy using an earlier version of the device for 45 minutes a day, for two months. “The data points to faster recovery of the treated group, indicating that BRAIN.Q’s treatment may not only improve the overall recovery after stroke, but also shorten the recovery period. We hope to test this hypothesis in our ongoing clinical trial,” says Segal. “Some recovered dramatically in the first month, some in the second, depending on how injured the brain was. “People regained everyday function so that they didn’t need help with eating or changing clothes or bathing. “After two months of treatment someone who couldn’t move their legs and was in a wheelchair could walk. Sometimes with a stick, but they could walk.” Tools to fix the problem Stroke is a leading cause of adult disability worldwide. BRAIN.Q’s treatment reduces disability and enhances the potential for recovery. “We are affecting the brain directly, but in a non-invasive manner,” says Segal. “We are affecting the ability of the brain to regenerate connections between cells. “I don’t want to push the brain to do something that it can’t do by itself. I want to harness its natural pattern of waves,” he explains. “You can take a tow truck and drive your broken car all around the city. But I want to take it to the mechanic who will use simple tools and fix the problem.” How did he feel when he saw how the first patients had recovered? “I wanted to cry,” he says. He goes on to relate the story of a woman in Israel who suffered a spinal cord injury in a car crash and has regained control of her legs and bowels, thanks to BRAIN.Q. And there are many more examples. BRAIN.Q, based at the Hebrew University’s Givat Ram campus in Jerusalem, is now conducting trials of the investigational device at patients’ homes after they’ve been discharged from the hospital. “In the beginning I was the CEO because there was nobody else in the company,” says Segal. “Then I became the chief technical officer and now I’m chief of innovation because I think this is where I’m doing the best work I can do.” Can he help his son? Although his son Lear’s diagnosis set him on this journey, Segal eventually honed in on treating strokes because, in neurological terms, they are less complex than familial dysautonomia (also known as Riley-Day syndrome). Familial dysautonomia, particularly prevalent among individuals of Ashkenazi Jewish descent, affects the autonomic nervous system that controls involuntary bodily functions such as breathing, swallowing, digestion, tear production and muscle stability. Lear doesn’t have natural tears, can’t drink liquids, has to eat condensed food, and needs to be held while attempting to walk. In addition, he had spinal fusion surgery at the age of 10. “The most serious situation is when he is in crisis, meaning that whenever he has stress, his autonomic nervous system tries to balance his blood pressure, temperature and chemical balance, and fails. His body goes into ‘panic’ conditions, very similar to those when a normal person is bitten by a snake — he starts to vomit, his blood pressure skyrockets, his temperature increases,” Segal says. “The only way to help him is using medication that brings his autonomic nervous system to a halt, causing it to reset and resume normal operation.” Segal is hopeful that, in time, BRAIN.Q will find a way to re-grow neural links in people with this condition. Meanwhile, he is gratified that the technology can aid stroke patients. For more information, click here. To read the original article click here.

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Combat Cognitive Decline and Grow New Brain Cells with an Intriguing Mineral

The AHA! Team — Wed, 07 Aug 2024 08:50:37 +0000

Lori Alton via NaturalHealth365 – At its mildest – which may involve occasional “blanking” on names or temporarily misplacing car keys – it causes embarrassment, annoyance, or minor inconvenience. At its worst, it is debilitating, jeopardizing the ability to read, write, and talk and threatening one’s ability to live independently. We are speaking, of course, of cognitive decline. Sometimes called cognitive impairment, this age-related condition is characterized by a decrease in the ability to learn, remember, and concentrate. There is currently no cure for cognitive decline, and ongoing research focuses on therapies and treatments intended to alleviate it or slow its progress. Recent research has illuminated the ability of selenium, an essential trace mineral, to help maintain healthy cognitive function – and potentially combat cognitive impairment. What functions does selenium perform in the body? Selenium is an important constituent of selenoproteins, a group of compounds needed for antioxidant defense, DNA synthesis, and thyroid hormone metabolism. (In fact, glutathione, the body’s “master” antioxidant and neutralizer of toxins, is one of the primary selenoproteins). Because selenium combats oxidative damage and inflammation in the brain, it is believed to play an important role in protecting brain health. And this mineral may even take the protection of cognitive function to the “next level.” In recent studies, it has been found to promote neurogenesis – the formation of new brain cells – in the hippocampus, an area of the brain linked with learning and memory. Warning: Low levels are linked to neurodegenerative conditions Like so many health-sustaining compounds, selenium is normally present in good supply in young people but becomes scarcer with age. Researchers have observed that the risk of cognitive decline and Alzheimer’s disease rises as selenium levels fall. In a 2023 meta-analysis published in Nutrients, the authors concluded that people with neurodegenerative diseases have lower levels. These shortfalls can have grave consequences. For example, preliminary studies have suggested that selenium deficiency causes brain inflammation. Conversely, animal studies have shown that increasing intake can reduce the accumulation of harmful tau and beta-amyloid proteins linked with Alzheimer’s disease. The “million-dollar question:” Can selenium improve age-related cognitive decline? Research has yielded encouraging results. Preliminary studies have shown that treating cultured brain cells with selenium led to increases in proliferation and signs of neurogenesis. A separate study showed that adding supplementary selenium directly to the drinking water of elderly mice caused significant improvements in learning and memory. Clearly, cell and animal studies offer valuable data on the potential of this micronutrient. But what about human studies? In a study published in 2023 in the Journal of Cardiac Failure involving patients with congestive heart failure, participants with higher levels of selenoproteins (which, in turn, indicate selenium levels) performed better on global cognitive tests than those with lower levels. This seemed to echo the findings of an earlier study published in Epidemiology that showed better cognitive performance among older adults with increased levels of selenium. Another study published in the European Journal of Nutrition showed that supplementing with a single selenium-packed Brazil nut improved verbal fluency and mental function in patients with mild cognitive impairment. However, other research has shown mixed results, and more studies are needed. It’s worth noting that selenium can also promote heart health and discourage atherosclerosis. A review involving over 433,000 participants with coronary heart disease showed that supplementation decreased levels of inflammatory C-reactive protein while increasing levels of glutathione. How much is too much? While serious selenium deficiencies are uncommon in the United States, holistic practitioners note that inadequate intake can occur in vegetarians, vegans, and others who consume little meat and seafood. Consuming food grown in soil with low selenium levels can also cause shortfalls. The Office of Dietary Supplements recommends 55 micrograms of selenium daily for adults. You can increase your intake by eating oysters, poultry, beef, cold-water fatty fish, and eggs. However, the undisputed “heavyweight” of selenium content is the Brazil nut, with a single ounce (six or seven nuts) delivering a whopping 544 micrograms. Incidentally, there is such a thing as “too much selenium.” Symptoms of excessive intake include skin rash, nausea, diarrhea, fatigue, and irritability. Acute selenium toxicity, a more serious condition, can lead to tremors, acute respiratory distress syndrome, organ failure, and even death. The Food and Nutrition Board has established a daily upper limit for selenium (from food and supplements combined) of 400 mcg for adults. (Caution – Brazil nuts could cause toxicity if consumed in excessive amounts. A mere half dozen Brazil nuts, in one sitting, could exceed the tolerable upper limit for the day. Limiting yourself to no more than 3 of these tasty, nutritious nuts a day allows you to rack up healthy levels of this essential trace mineral without risk of toxicity.) Selenium is available as a supplement, with typical amounts ranging from 50 to 400 micrograms a day. However, consult with your holistic doctor before supplementing. Remember: Other steps to protect cognitive function include proper nutrition, staying physically and mentally active, and maintaining a healthy social network. The latest research suggests that selenium may help you retain sharp mental function while safeguarding your priceless memories well into old age. It’s certainly wise to ensure you have adequate amounts of this valuable micronutrient. Sources for this article include: NIH.gov LifeExtension.com NIH.gov OfficeofDietarySupplements.gov NIH.gov NIH.gov Springer.com VeryWellHealth.com To read the original article click here.

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Breakthrough UC San Diego Brain Recording Device Receives FDA Approval for a Clinical Trial

The AHA! Team — Fri, 02 Aug 2024 08:21:00 +0000

University of California San Diego via Newswise – The Federal Drug Administration approved a clinical trial to test the effectiveness of an electronic grid that records brain activity during surgery, developed by engineers at the University of California San Diego. The device with nanoscale sensors records electrical signals directly from the surface of the human brain in record-breaking detail. The grid’s breakthrough resolution could provide better guidance for planning and performing surgeries to remove brain tumors and treat drug-resistant epilepsy. The grid’s higher resolution for recording brain signals could improve neurosurgeons’ ability to minimize damage to healthy brain tissue. During epilepsy surgery, the novel grid could improve the ability to precisely identify the regions of the brain where epileptic seizures originate for safe and effective treatment. The new brain sensor array, known as platinum nanorod grid (PtNRGrid) features a densely packed grid of a record-breaking 1,024 embedded electrocorticography (ECoG) sensors. The device rests on the surface of the brain and is approximately 6 microns thin–smaller than one tenth of the human hair–and flexible. As a result, it can both adhere and conform to the surface of the brain, bending as the brain moves while providing high-quality, high-resolution recordings of brain activity. In contrast, the ECoG grids most commonly used in surgeries today typically have between 16 and 64 sensors. These grids are rigid, stiffer and more than 0.5 mm in thickness and do not conform to the curved surface of the brain. The PtNRGrid was invented by Shadi Dayeh, a Professor in the Department of Electrical and Computer Engineering at the University of California San Diego and members of his team. Over the years, the team developed the PtNRGrid technology in collaboration with neurosurgeons and medical researchers from UC San Diego, Massachusetts General Hospital (MGH) and Oregon Health & Science University (OHSU). “This accomplishment ushers in a new era of clinical neuroscience and neuromonitoring,” Dayeh said. “We are very excited to receive the FDA approval to apply our groundbreaking PtNRGrid in a clinical setting. It is a credit to the hard work of my team members who worked tirelessly to meet the quality criteria mandated by the FDA. I am also grateful to my clinical partners, the support of the NIH, and to the campus leadership that fostered an impactful ecosystem across engineering and medicine to transform the future of healthcare.” The FDA approved an investigational device exemption (IDE) for a “pivotal study [titled] “Systematic Evaluation of Platinum Nanorod Grids (PtNRGrids) for Intraoperative Mapping and Neurophysiological Monitoring (IONM) During Brain Surgeries.” Specifically, the clinical trial is designed to demonstrate the effectiveness of the PtNRGrid device to map both normal and pathological brain activity. During the trial, UC San Diego engineers will partner with clinician-scientists: Drs. Sharona Ben-Haim and Eric Halgren at UC San Diego, Dr. Sydney Cash at MGH, and Dr. Ahmed Raslan at OHSU. In a first phase, surgeons will implant the PtNRGrid in 20 patients, then measure and compare the grid’s performance with the present state-of-the-art. The PtNRGrid will be deployed in surgeries to remove brain tumors and to remove tissue that causes epileptic seizures. Record-breaking density Dayeh’s team has pioneered human brain and spinal cord mapping with thousands of channels since 2019, and has reported early safety and efficacy results in a series of articles published in Science Translational Medicine in 2022 in human subjects. PtNRGrid is the only device with thousands of channels to demonstrate in peer-reviewed publications that it can map motor and language brain activity, as well as epileptic discharges, by producing panoramic videos of brain waves over 10 square centimeters of the brain’s cortex while maintaining resolution at a microscopic level. Currently, Dayeh’s research group holds the world record of recording brain activity from a single cortical grid with 2,048 channels on the surface of the human brain published in Science Translational Medicine in 2022. The device was used in the operating room of Dr. Ahmed Raslan of the OHSU. Since then, the team has increased the number of recording channels to 4,096 and continues to work on increasing the number of channels in the grid to monitor brain activity in even higher resolution. Pending success of this staged trial, the team will transition to the next crucial step of making the PtNRGrid available for commercial use at scale. Demonstrating that ECoG grids with sensors in the thousands of channels record brain activity with high fidelity also opens new opportunities in neuroscience for uncovering a deeper understanding of how the human brain functions. Basic science advances, in turn, could lead to improved treatments grounded in enhanced understanding of brain function. “Our goal is to provide a new atlas for understanding and treating neurological disorders, working with a network of highly experienced clinical collaborators at UC San Diego, MGH, and OHSU,” Dayeh said. Dayeh’s work toward the FDA approval is supported by an NIH BRAIN® Initiative award # UG3NS123723. To read the original article click here.

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