Chapter 3. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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By Tina Hesman Saey One particular retrovirus — embedded in the DNA of jawed vertebrates — helps turn on production of a protein needed to insulate nerve fibers, researchers report February 15 in Cell. Such insulation, called myelin, may have helped make speedy thoughts and complex brains possible. The retrovirus trick was so handy, in fact, that it showed up many times in the evolution of vertebrates with jaws, the team found. Retroviruses — also known as jumping genes or retrotransposons — are RNA viruses that make DNA copies of themselves to embed in a host’s DNA. Scientists once thought of remnants of ancient viruses as genetic garbage, but that impression is changing, says neuroscientist Jason Shepherd, who was not involved in the study. “We’re finding more and more that these retrotransposons and retroviruses have influenced the evolution of life on the planet,” says Shepherd, of the University of Utah Spencer Fox Eccles School of Medicine in Salt Lake City. Remains of retroviruses were already known to have aided the evolution of the placenta, the immune system and other important milestones in human evolution (SN: 5/16/17). Now, they’re implicated in helping to produce myelin. Myelin is a coating of fat and protein that encases long nerve fibers known as axons. The coating works a bit like the insulation around an electrical wire: Nerves sheathed in myelin can send electrical signals faster than uninsulated nerves can. © Society for Science & the Public 2000–2024.

Keyword: Glia; Evolution
Link ID: 29154 - Posted: 02.20.2024

By Jyoti Madhusoodanan On July 12, 2015, Elena Daly was packing for a family vacation when she walked into her 16-year-old son’s room and found him unconscious. Her son, Max, had overdosed on opioids, aspirated vomit, and fallen into a coma. By that point, Max had struggled with addiction for about three years. He had tried medication, therapy, and residential treatment programs in France, where the family lives, as well as in the United States and the United Kingdom. In fact, his July relapse occurred just days after returning home from a six-month stint in an in-patient rehab program. The coma lasted three days and worsened a pre-existing movement disorder to a degree where Max was unable to attend high school. “I couldn’t hold a pen without throwing it across the room or hold a cup of coffee without spilling it on myself,” he recently recalled. Max’s struggles with opioid use are not unusual: An estimated 40 to 60 percent of people who have an addiction experience relapse after treatment. Some researchers have suggested that a substantial portion of those who relapse suffer from what might be considered a “treatment-resistant” form of the disorder, though that condition is not formally recognized as a medical diagnosis. In recent years, scientists have explored treating these intractable cases of opioid dependence with deep brain stimulation, an intervention that entails surgically implanting an electrode into a precisely determined region of the brain, where it delivers regular pulses to control problematic electric signals. The surgery has proven effective for neurological conditions such as Parkinson’s disease and essential tremor, a disorder that can cause a person’s limbs, head, trunk, and voice to quake. But for researchers attempting to study its efficacy for addiction, the procedure’s invasiveness and cost — typically in the hundreds of thousands of dollars — have raised steep hurdles. Work in the field has largely been limited to one-off treatments and small studies with one or a few participants, making it tough to ascertain how many people globally have received the treatment or how successful it has been for them.

Keyword: Drug Abuse
Link ID: 29121 - Posted: 01.31.2024

By Carl Zimmer Multiple sclerosis, an autoimmune disease that affects 2.9 million people, presents a biological puzzle. Many researchers suspect that the disease is triggered by a virus, known as Epstein-Barr, which causes the immune system to attack the nerves and can leave patients struggling to walk or talk. But the virus can’t be the whole story, since nearly everyone is infected with it at some point in life. A new study found a possible solution to this paradox in the skeletal remains of a lost tribe of nomads who herded cattle across the steppes of western Asia 5,000 years ago. It turns out that the nomads carried genetic mutations that most likely protected them from pathogens carried by their animals, but that also made their immune systems more sensitive. These genes, the study suggests, made the nomads’ descendants prone to a runaway immune response. The finding is part of a larger, unprecedented effort to understand how the evolutionary past has shaped the health of living people. Researchers are analyzing thousands of genomes of people who lived between Portugal and Siberia and between Norway and Iran roughly 3,000 to 11,000 years ago. They hope to trace the genetic roots of not only multiple sclerosis, but also diabetes, schizophrenia and many other modern illnesses. “We are taking ancient human genomics to a whole new level,” said Eske Willerslev, a geneticist at the University of Copenhagen who led the effort. The researchers published the multiple sclerosis study as well as three other papers on the genetics and health of ancient peoples on Wednesday in the journal Nature. For more than a decade, Dr. Willerslev and other researchers have been pulling DNA from ancient human bones. By comparing the surviving genetic material with that of living people, the scientists have been able to track some of the most significant migrations of people across the world. © 2024 The New York Times Company

Keyword: Multiple Sclerosis; Evolution
Link ID: 29093 - Posted: 01.11.2024

Kamal Nahas Peter Hegemann, a biophysicist at Humboldt University, has spent his career exploring interactions between proteins and light. Specifically, he studies how photoreceptors detect and respond to light, focusing largely on rhodopsins, a family of membrane photoreceptors in animals, plants, fungi, protists, and prokaryotes.1 Early in his career, his curiosity led him to an unknown rhodopsin in green algae that later proved to have useful applications in neuroscience research. Hegemann became a pioneer in the field of optogenetics, which revolutionized the ways in which scientists draw causal links between neuronal activity and behavior. In the early 1980s during his graduate studies at the Max Planck Institute of Biochemistry, Hegemann spent his days exploring rhodopsins in bacteria and archaea. However, the field was crowded, and he was eager to study a rhodopsin that scientists knew nothing about. Around this time, Kenneth Foster, a biophysicist at Syracuse University, was investigating whether the green algae Chlamydomonas, a photosynthetic unicellular eukaryote related to plants, used a rhodopsin in its eyespot organelle to detect light and trigger the algae to swim. He struggled to pinpoint the protein itself, so he took a roundabout approach and started interfering with nearby molecules that interact with rhodopsins.2 Rhodopsins require the small molecule retinal to function as a photoreceptor. When Foster depleted Chlamydomonas of its own retinal, the algae were unable to use light to direct movement, a behavior that was restored when he introduced retinal analogues. In 1985, Hegemann joined Foster’s group as a postdoctoral researcher to continue this work. “I wanted to find something new,” Hegemann said. “Therefore, I worked on an exotic organism and an exotic topic.” A year later, Hegemann started his own research group at the Max Planck Institute of Biochemistry where he searched for the green algae’s rhodopsin that Foster proposed should exist. © 1986–2024 The Scientist.

Keyword: Brain imaging; Vision
Link ID: 29077 - Posted: 01.03.2024

Sydney E. Smith When most people hear about electroconvulsive therapy, or ECT, it typically conjures terrifying images of cruel, outdated and pseudo-medical procedures. Formerly known as electroshock therapy, this perception of ECT as dangerous and ineffective has been reinforced in pop culture for decades – think the 1962 novel-turned-Oscar-winning film “One Flew Over the Cuckoo’s Nest,” where an unruly patient is subjected to ECT as punishment by a tyrannical nurse. Despite this stigma, ECT is a highly effective treatment for depression – up to 80% of patients experience at least a 50% reduction in symptom severity. For one of the most disabling illnesses around the world, I think it’s surprising that ECT is rarely used to treat depression. Contributing to the stigma around ECT, psychiatrists still don’t know exactly how it heals a depressed person’s brain. ECT involves using highly controlled doses of electricity to induce a brief seizure under anesthesia. Often, the best description you’ll hear from a physician on why that brief seizure can alleviate depression symptoms is that ECT “resets” the brain – an answer that can be fuzzy and unsettling to some. As a data-obsessed neuroscientist, I was also dissatisfied with this explanation. In our newly published research, my colleagues and I in the lab of Bradley Voytek at UC San Diego discovered that ECT might work by resetting the brain’s electrical background noise. To study how ECT treats depression, my team and I used a device called an electroencephalogram, or EEG. It measures the brain’s electrical activity – or brain waves – via electrodes placed on the scalp. You can think of brain waves as music played by an orchestra. Orchestral music is the sum of many instruments together, much like EEG readings are the sum of the electrical activity of millions of brain cells. © 2010–2023, The Conversation US, Inc.

Keyword: Depression
Link ID: 29036 - Posted: 12.09.2023

By Carl Zimmer Traumatic brain injuries have left more than five million Americans permanently disabled. They have trouble focusing on even simple tasks and often have to quit jobs or drop out of school. A study published on Monday has offered them a glimpse of hope. Five people with moderate to severe brain injuries had electrodes implanted in their heads. As the electrodes stimulated their brains, their performance on cognitive tests improved. If the results hold up in larger clinical trials, the implants could become the first effective therapy for chronic brain injuries, the researchers said. “This is the first evidence that you can move the dial for this problem,” said Dr. Nicholas Schiff, a neurologist at Weill Cornell Medicine in New York who led the study. Gina Arata, one of the volunteers who received the implant, was 22 when a car crash left her with fatigue, memory problems and uncontrollable emotions. She abandoned her plans for law school and lived with her parents in Modesto, Calif., unable to keep down a job. In 2018, 18 years after the crash, Ms. Arata received the implant. Her life has changed profoundly, she said. “I can be a normal human being and have a conversation,” she said. “It’s kind of amazing how I’ve seen myself improve.” Dr. Schiff and his colleagues designed the trial based on years of research on the structure of the brain. Those studies suggested that our ability to focus on tasks depends on a network of brain regions that are linked to each other by long branches of neurons. The regions send signals to each other, creating a feedback loop that keeps the whole network active. Sudden jostling of the brain — in a car crash or a fall, for example — can break some of the long-distance connections in the network and lead people to fall into a coma, Dr. Schiff and his colleagues have hypothesized. During recovery, the network may be able to power itself back up. But if the brain is severely damaged, it may not fully rebound. Dr. Schiff and his colleagues pinpointed a structure deep inside the brain as a crucial hub in the network. Known as the central lateral nucleus, it is a thin sheet of neurons about the size and shape of an almond shell. © 2023 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 29033 - Posted: 12.06.2023

By Simon Makin Our thoughts and feelings arise from networks of neurons, brain cells that send signals using chemicals called neurotransmitters. But neurons aren't alone. They're supported by other cells called glia (Greek for “glue”), which were once thought to hold nerve tissue together. Today glia are known to help regulate metabolism, protect neurons and clean up cellular waste—critical but unglamorous roles. Now, however, neuroscientists have discovered a type of “hybrid” glia that sends signals using glutamate, the brain's most common neurotransmitter. These findings, published in Nature, breach the rigid divide between signaling neurons and supportive glia. “I hope it's a boost for the field to move forward, to maybe begin studying why certain [brain] circuits have this input and others don't,” says study co-author Andrea Volterra, a neuroscientist at the University of Lausanne in Switzerland. Around 30 years ago researchers began reporting that star-shaped glia called astrocytes could communicate with neurons. The idea was controversial, and further research produced contradictory results. To resolve the debate, Volterra and his team analyzed existing data from mouse brains. These data were gathered using a technique called single-cell RNA sequencing, which lets researchers catalog individual cells' molecular profiles instead of averaging them in a bulk tissue sample. Of nine types of astrocytes they found in the hippocampus—a key memory region—one had the cellular machinery required to send glutamate signals. The small numbers of these cells, present only in certain regions, may explain why earlier research missed them. “It's quite convincing,” says neuroscientist Nicola Hamilton-Whitaker of King's College London, who was not involved in the study. “The reason some people may not have seen these specialized functions is they were studying different astrocytes.” © 2023 SCIENTIFIC AMERICAN,

Keyword: Glia
Link ID: 29025 - Posted: 11.26.2023

By Erin Garcia de Jesús A new brain-monitoring device aims to be the Goldilocks of anesthesia delivery, dispensing drugs in just the right dose. No physician wants a patient to wake up during surgery — nor do patients. So anesthesiologists often give more drug than necessary to keep patients sedated during medical procedures or while on lifesaving machines like ventilators. But anesthetics can sometimes be harmful when given in excess, says David Mintz, an anesthesiologist at Johns Hopkins University. For instance, elderly people with cognitive conditions like dementia or age-related cognitive decline may be at higher risk of post-surgical confusion. Studies also hint that long periods of use in young children might cause behavioral problems. “The less we give of them, the better,” Mintz says. An automated anesthesia delivery system could help doctors find the right drug dose. The new device monitored rhesus macaques’ brain activity and supplied a common anesthetic called propofol in doses that were automatically adjusted every 20 seconds. Fluctuating doses ensured the animals received just enough drug — not too much or too little — to stay sedated for 125 minutes, researchers reported October 31 in PNAS Nexus. The study is a step toward devising and testing a system that would work for people. © Society for Science & the Public 2000–2023.

Keyword: Consciousness; Pain & Touch
Link ID: 29021 - Posted: 11.26.2023

By Laura Dattaro A brain is nothing if not communicative. Neurons are the chatterboxes of this conversational organ, and they speak with one another by exchanging pulses of electricity using chemical messengers called neurotransmitters. By repeating this process billions of times per second, a brain converts clusters of chemicals into coordinated actions, memories and thoughts. Researchers study how the brain works by eavesdropping on that chemical conversation. But neurons talk so loudly and often that if there are other, quieter voices, it might be hard to hear them. For most of the 20th century, neuroscientists largely agreed that neurons are the only brain cells that propagate electrical signals. All the other brain cells, called glia, were thought to serve purely supportive roles. Then, in 1990, a curious phenomenon emerged: Researchers observed an astrocyte, a subtype of glial cell, responding to glutamate, the main neurotransmitter that generates electrical activity. In the decades since, research teams have come up with conflicting evidence, some reporting that astrocytes signal, and others retorting that they definitely do not. The disagreement played out at conferences and in review after review of the evidence. The two sides seemed irreconcilable. A new paper published in Nature in September presents the best proof yet that astrocytes can signal, gathered over eight years by a team co-led by Andrea Volterra, visiting faculty at the Wyss Center for Bio and Neuro Engineering in Geneva, Switzerland. The study includes two key pieces of evidence: images of glutamate flowing from astrocytes, and genetic data suggesting that these cells, dubbed glutamatergic astrocytes, have the cellular machinery to use glutamate the way neurons do. The paper also helps explain the decades of contradictory findings. Because only some astrocytes can perform this signaling, both sides of the controversy are, in a sense, right: A researcher’s results depend on which astrocytes they sampled. All Rights Reserved © 2023

Keyword: Glia
Link ID: 28972 - Posted: 10.25.2023

by Angie Voyles Askham About once a month throughout 2012, researchers from four labs at the University of California, San Francisco filed into a conference room in the early morning to hear the latest news on their ambitious project. The heads of the labs — Arturo Alvarez-Buylla, Scott Baraban, Arnold Kriegstein and John Rubenstein — had formed the company Neurona Therapeutics in 2008 to develop a new approach to treating neurological conditions, using cell therapy. Their goal was to transplant inhibitory interneurons into people’s nervous systems to treat the overexcited circuits that can give rise to conditions such as epilepsy, Alzheimer’s disease and neuropathic pain. These meetings had grown tense as researchers within the four groups struggled to see eye to eye on data interpretation, particularly when Cory Nicholas, then a postdoctoral researcher in Kriegstein’s lab, presented his protocol for producing the inhibitory interneurons. On those days, Nicholas would open his slide deck to reveal images of fluorescent cells on a large screen behind him — red and white branching blobs against a black background. Then the questions would come from Baraban’s group. Why do some of the cells seem to be the wrong kind? Are they forming tumors? Can we see the neighboring images? There were some in the audience who thought they were being shown only the best images, says Joy Sebe, a postdoc in Baraban’s lab at the time. Nicholas, for his part, says he welcomed the questioning — in science, he says, “your job is to challenge” — and Daniel Vogt, who was a postdoc Rubenstein’s lab at the time, says the back and forth was simply part of the scientific process. © 2023 Simons Foundation

Keyword: Epilepsy
Link ID: 28948 - Posted: 10.07.2023

Max Kozlov Doctors measure blood pressure to track heart disease, and scrutinize insulin levels in people with diabetes. But when it comes to depression, clinicians must rely on people’s self-reported symptoms, making it difficult to objectively measure a treatment’s effects. Now, researchers have used artificial intelligence (AI) to identify a brain signal linked to recovery from depression in people treated with deep-brain stimulation (DBS), a technique that uses electrodes implanted into the brain to deliver electric pulses that alter neural activity. The team reported1 its results on ten people with severe depression, in Nature on 20 September. If replicated in a larger sample, these findings could represent a “game-changer in how we would be able to treat depression”, says Paul Holtzheimer, a neuroscientist at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire, who was not involved in the research. Efforts to treat depression with DBS have so far had limited success: two randomized-controlled trials2,3 failed to demonstrate a benefit compared with a placebo. One problem, says Helen Mayberg, a neurologist at Icahn School of Medicine at Mount Sinai in New York City, and a co-author of the Nature paper, is that doctors only have access to self-reported data to assess whether a person’s stimulation voltage needs adjustment. With self-reported data, clinicians have a difficult time distinguishing between normal, day-to-day mood fluctuations and pathological depression, says Todd Herrington, director of the DBS programme at Massachusetts General Hospital in Boston, who was not involved in the research. To find a more objective measure of depression recovery, Mayberg and her colleagues developed a DBS device that includes sensors to measure brain activity, as well as the standard electrodes for brain stimulation. They implanted this device into the subcallosal cingulate cortex — an area of the brain that has a role in regulating emotional behaviour — in ten people with depression that resisted all forms of treatment. © 2023 Springer Nature Limited

Keyword: Depression; Brain imaging
Link ID: 28932 - Posted: 09.27.2023

by Maris Fessenden A new lightweight device with a wisplike tether can record neural activity while mice jump, run and explore their environment. The open-source recording system, which its creators call ONIX, overcomes several of the limitations of previous systems and enables the rodents to move more freely during recording. The behavior that ONIX allows brings to mind children running around in a playground, says Jakob Voigts, a researcher at the Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Virginia, who helped build and test the system. He and his colleagues describe their work in a preprint posted on bioRxiv earlier this month. To understand how the brain creates complex behaviors — such as those found in social interaction, sensory processing and cognition, which are commonly affected in autism — researchers observe brain signals as these behaviors unfold. Head-mounted devices enable researchers to eavesdrop on the electrical chatter between brain cells in mice, rats and primates. But as the smallest of these animal models, mice present some significant challenges. Current neural recording systems are bulky and heavy, making the animals carry up to a fifth of their body weight on their skulls. Predictably, this slows the mice down and tires them out. And most neural recording systems use a tether to relay signals from the mouse’s brain to a computer. But this tether twists and tangles as the mouse turns its head and body, exerting torque that the mouse can feel. Researchers must therefore periodically replace or untangle the tether. Longer tethers allow for more time to elapse between changeouts, but the interruptions still affect natural behavior. And battery-powered, wireless systems add too much weight. Altogether, these challenges inhibit natural behaviors and limit the amount of time that recording can take place, preventing scientists from studying, for example, the complete process of learning a new task. © 2023 Simons Foundation

Keyword: Brain imaging
Link ID: 28930 - Posted: 09.27.2023

By Laura Sanders On a hot, sunny Sunday afternoon in Manhattan, time froze for Jon Nelson. He stood on the sidewalk and said good-bye to his three kids, whose grandfather had come into the city from Long Island to pick them up. Like any parent, Jon is deeply attuned to his children’s quirks. His oldest? Sometimes quiet but bitingly funny. His middle kid? Rates dad a 10 out of 10 on the embarrassment scale and doesn’t need a hug. His 10-year-old son, the baby of the family, is the emotional one. “My youngest son would climb back up into my wife’s womb if he could,” Jon says. “He’s that kid.” An unexpected parade had snarled traffic, so Jon parked illegally along a yellow curb on 36th Street, near where his father-in-law was waiting. It was time to go. His youngest gave the last hug. “He looked up, scared and sad,” Jon says, and asked, “Dad, am I going to see you again?” That question stopped the clock. “I was like, ‘Oh man,’” Jon says. “It was one of those moments where I was living it through his eyes. And I got scared for the first time.” Until that good-bye, Jon hadn’t wanted to live. For years, he had a constant yearning to die — he talks about it like it was an addiction — as he fought deep, debilitating depression. But his son’s question pierced through that heaviness and reached something inside him. “That was the first time I really thought about it. I was like, ‘I kind of hope I don’t die.’ I hadn’t had that feeling in so long.” That hug happened around 5 p.m. on August 21, 2022. Twelve hours later, Jon was wheeled into a surgical suite. There, at Mount Sinai’s hospital just southwest of Central Park, surgery team members screwed Jon’s head into a frame to hold it still. Then they numbed him and drilled two small holes through the top of his skull, one on each side. Through each hole, a surgeon plunged a long, thin wire dotted at the end with electrodes deep into his brain. The wiring, threaded under his skin, snaked around the outside of Jon’s skull and sank down behind his ear. From there, a wire wrapped around to the front, meeting a battery-powered control box that surgeons implanted in his chest, just below his collarbone. © Society for Science & the Public 2000–2023.

Keyword: Depression
Link ID: 28924 - Posted: 09.23.2023

By Phil Jaekl In the mid-1970s, a British researcher named Anthony Barker wanted to measure the speed at which electrical signals travel down the long, slender nerves that can carry signals from the brain to muscles like those in the hand, triggering movement. To find out, he needed a way to stimulate nerves in people. Researchers had already used electrodes placed on the skin to generate a magnetic field that penetrated human tissue — this produced an electric current that activated the peripheral nerves in the limbs. But the technique was painful, burning the skin. Barker, at the University of Sheffield in England, and his colleagues started to work on a better method. In 1985, with promising results under their belts, they tried positioning the coil-shaped magnetic device they’d developed on participants’ heads. The coil emitted rapidly alternating magnetic pulses over the brain region that controls movement, generating weak electrical currents in the brain tissue and activating neurons that control muscles in the hand. After about 20 milliseconds, the participants’ fingers twitched. The technique, now called transcranial magnetic stimulation (TMS), has proved a vital tool for investigating how the human brain works. When targeted to specific brain regions, TMS can temporarily inhibit or enhance various functions – blocking the ability to speak, for instance, or making it easier to commit a series of numbers to memory. And when brain imaging technologies such as functional magnetic resonance imaging (fMRI) emerged in the 1990s, researchers could now “see” inside people’s brains as they received TMS stimulation. They could also observe how neural pathways respond differently to stimulation in psychiatric illnesses like schizophrenia and depression. In recent decades, this fundamental research has yielded new treatments that alter brain activity, with TMS therapies for depression at the fore. In 2008, the US Food and Drug Administration approved NeuroStar, the nation’s first TMS depression device, and many other countries have since sanctioned the approach. Yet even though TMS is now a widely available depression treatment, many questions remain about the method. It’s not clear how long the benefits of TMS can last, for example, or why it appears to work for some people with depression but not others. Another challenge is disentangling the effects of TMS from the placebo effect — when someone believes that they will benefit from treatment and gets better even though they’re receiving a “sham” form of stimulation. © 2023 Annual Reviews

Keyword: Depression
Link ID: 28903 - Posted: 09.10.2023

Neurotransmitters are the words our brain cells use to communicate with one another. For years, researchers relied on tools that provided limited temporal and spatial resolution to track changes in the fast chemical chat between neurons. But that started to change about ten years ago for glutamate—the most abundant excitatory neurotransmitter in vertebrates that plays an essential role in learning, memory, and information processing—when scientists engineered the first glutamate fluorescent reporter, iGluSnFR, which provided a readout of neurons’ fast glutamate release. In 2013, researchers at the Howard Hughes Medical Institute collaborated with scientists from other institutions to develop the first generation of iGluSnFR.1 To create the biosensor, the team combined a bacteria-derived glutamate binding protein, Gltl, a wedged fluorescent GFP protein, and a membrane-targeting protein that anchors the reporter to the surface of the cell. Upon glutamate binding, the Gltl protein changes its conformation, increasing the fluorescence intensity of GFP. In their first study, the team showcased the utility of the biosensor for monitoring glutamate levels by demonstrating selective activation by glutamate in cell cultures. By conducting experiments with brain cells from the C. elegans worm, zebrafish, and mice, they confirmed that the reporter also tracked glutamate in vivo, a finding that set iGluSnFR apart from existing glutamate sensors. The first iGluSnFR generation allowed researchers to study glutamate dynamics in different biological systems, but the indicator could not detect small amounts of the neurotransmitter or keep up with brain cells’ fast glutamate release bouts. Making improvements © 1986–2023 The Scientist.

Keyword: Brain imaging
Link ID: 28901 - Posted: 09.10.2023

By Claudia López Lloreda Cells hidden in the skull may point to a way to detect, diagnose and treat inflamed brains. A detailed look at the skull reveals that bone marrow cells there change and are recruited to the brain after injury, possibly traveling through tiny channels connecting the skull and the outer protective layer of the brain. Paired with the discovery that inflammation in the skull is disease-specific, these new findings collectively suggest the skull’s marrow could serve as a target to track and potentially treat neurological disorders involving brain inflammation, researchers report August 9 in Cell. Immune cells that infiltrate the central nervous system during many diseases and neuronal injury can wreak havoc by flooding the brain with damaging molecules. This influx of immune cells causes inflammation in the brain and spinal cord and can contribute to diseases like multiple sclerosis (SN: 11/26/19). Detecting and dampening this reaction has been an extensive field of research. With this new work, the skull, “something that has been considered as just protective, suddenly becomes a very active site of interaction with the brain, not only responding to brain diseases, but also changing itself in response to brain diseases,” says Gerd Meyer zu Hörste, a neurologist at University of Münster in Germany who was not involved in the study. Ali Ertürk of the Helmholtz Center in Munich and colleagues discovered this potential role for the skull while probing the idea that the cells in skull marrow might behave differently from those in other bones. Ertürk’s team compared the genetic activity of cells in mice skull marrow, and the proteins those cells made, with those in the rodent’s humerus, femur and four other bones, along with the meninges, the protective membranes between the skull and the brain. © Society for Science & the Public 2000–2023.

Keyword: Alzheimers; Multiple Sclerosis
Link ID: 28898 - Posted: 09.07.2023

Jon Hamilton If you've ever had trouble finding your keys or remembering what you had for breakfast, you know that short-term memory is far from perfect. For people who've had a traumatic brain injury (TBI), though, recalling recent events or conversations can be a major struggle. "We have patients whose family cannot leave them alone at home because they will turn on the stove and forget to turn it off," says Dr. Ramon Diaz-Arrastia, who directs the Traumatic Brain Injury Clinical Research Center at the University of Pennsylvania. So Arrastia and a team of scientists have been testing a potential treatment. It involves delivering a pulse of electricity to the brain at just the right time. And it worked in a study of eight people with moderate or severe TBIs, the team reports in the journal Brain Stimulation. A precisely timed pulse to a brain area just behind the ear improved recall by about 20 percent and reduced the person's memory deficit by about half. If the results pan out in a larger study, the approach might improve the lives of many young people who survive a serious TBI, says Diaz-Arrastia, an author of the study and a professor of neurology at Penn. "In many cases, the reason they're unable to rejoin and fully participate in society is because of their memory problems," he says. "And they often have this disability that goes on for many, many decades." But the treatment is not for the timid. It requires patients to have electrodes surgically implanted in their brain. And scientists are still refining the system that delivers the electrical pulses. More than 1.5 million people in the U.S. sustain a TBI each year. Common causes include falls, motor vehicle accidents, assaults, contact sports, and gunshots. © 2023 npr

Keyword: Brain Injury/Concussion
Link ID: 28870 - Posted: 08.09.2023

Max Kozlov Dead in California but alive in New Jersey: that was the status of 13-year-old Jahi McMath after physicians in Oakland, California, declared her brain dead in 2013, after complications from a tonsillectomy. Unhappy with the care that their daughter received and unwilling to remove life support, McMath’s family moved with her to New Jersey, where the law allowed them to lodge a religious objection to the declaration of brain death and keep McMath connected to life-support systems for another four and a half years. Prompted by such legal discrepancies and a growing number of lawsuits around the United States, a group of neurologists, physicians, lawyers and bioethicists is attempting to harmonize state laws surrounding the determination of death. They say that imprecise language in existing laws — as well as research done since the laws were passed — threatens to undermine public confidence in how death is defined worldwide. “It doesn’t really make a lot of sense,” says Ariane Lewis, a neurocritical care clinician at NYU Langone Health in New York City. “Death is something that should be a set, finite thing. It shouldn’t be something that’s left up to interpretation.” Since 2021, a committee in the Uniform Law Commission (ULC), a non-profit organization in Chicago, Illinois, that drafts model legislation for states to adopt, has been revising its recommendation for the legal determination of death. The drafting committee hopes to clarify the definition of brain death, determine whether consent is required to test for it, specify how to handle family objections and provide guidance on how to incorporate future changes to medical standards. The broader membership of the ULC will offer feedback on the first draft of the revised law at a meeting on 26 July. After members vote on it, the text could be ready for state legislatures to consider by the middle of next year. But as the ULC revision process has progressed, clinicians who were once eager to address these issues have become increasingly worried. © 2023 Springer Nature Limited

Keyword: Consciousness
Link ID: 28853 - Posted: 07.22.2023

By Stephanie Pappas Have you felt butterflies in your stomach or hunger pangs? Those “gut feelings” happen thanks to the vagus nerve, which is a superhighway that connects the brain and the gut. In recent years the vagus nerve has become an intriguing target for researchers looking to cure disorders of both the brain and the body. Vagus nerve stimulation—usually achieved with an electrode implanted in the neck to deliver electrical pulses directly to the nerve—is an approved treatment for epilepsy and some forms of depression. Scientists are now studying vagus nerve stimulation (VNS) for disorders such as rheumatoid arthritis and the inflammatory bowel disease Crohn’s. What gives this nerve such widespread impact? The vagus nerve is the longest of the cranial nerves, which emerge directly from the brain rather than traveling through the spinal cord. It begins at an opening at the base of the skull and runs down the neck and into the abdomen, where it collects signals from the viscera and helps regulate the automatic processes of the body, from digestion to sleep to inflammation. About 80 percent of its signals are sensory ones that travel from the inner organs up to the brain, while the other 20 percent travel from the brain to the body and regulate things such as intestinal contractions and heart rate. The vagus nerve is the key player in the parasympathetic nervous system, which is the “rest and digest” system that calms the body during times of low stress. “If you are relaxed, if you are sleeping, if you are in a restorative phase, it’s the vagus nerve dominating,” says Gregor Hasler, a psychiatrist at the University of Fribourg in Switzerland, who has written about the gut-brain connection.

Keyword: Depression; Epilepsy
Link ID: 28843 - Posted: 07.06.2023

Nicola Davis Science correspondent Researchers have discovered a genetic variant that appears to influence the speed at which multiple sclerosis (MS) progresses, potentially paving the way for new treatments. According to the MS International Federation, about 2.9 million people worldwide have MS, a condition in which the insulating coating of the nerves in the brain and spinal cord is damaged by the immune system. The nerve fibres themselves can also become damaged. While some people have a relapsing remitting form of the disease, others experience gradual progression that in some can cause severe disability. Researchers say they have identified a genetic variant that appears to increase the severity of the disease. They found that people who inherit the variant from both parents need a walking aid almost four years sooner than those without. “This is a very substantial effect for a single genetic variant,” said Sergio Baranzini, a professor of neurology at the University of California, San Francisco and co-senior author of the study. “Furthermore, this variant affects genes that are active in the central nervous system, a clear contrast to variants that confer risk [of MS], which overwhelmingly affect the immune system.” The study, published in the journal Nature, was an international endeavour, involving 70 institutions around the world. To make their discovery, the team analysed genetic data from more than 12,000 people with MS, screening more than 7m genetic variants for associations with the speed of disease progression. The team found that one variant, nestled between two genes called DYSF and ZNF638, was associated with a more rapid increase in disability. © 2023 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28840 - Posted: 07.01.2023