By Scientific American Custom Media Megan Hall: How does the stomach tell the brain it’s full? How do cells in our body grow and divide? James Rothman realized that the fundamental biology behind these processes are basically the same. In 2010, he shared The Kavli Prize in Neuroscience with Richard Scheller and Thomas Südhof for their work detailing how nerve cells communicate with each other on a microscopic level. Three years later, he received the Nobel Prize. Hall: James Rothman was pleasantly surprised when he received The Kavli Prize in Neuroscience. James Rothman: I'd always thought of myself as a biochemist first and a cell biologist second. And I never really thought of myself as a neuroscientist. Hall: He did apply to a neuroscience program in grad school… Rothman: It all just made a whole lot of sense, except for the fact that I wasn't admitted. Hall: But James is not the kind of person to worry about labels. In fact, he’s explored a range of scientific disciplines. As an undergrad at Yale, he studied physics, maybe in part because he grew up in the 50s. Rothman: Scientists and doctors were really the most admired in the 1950s. And it was the physicists in particular. Einstein, Oppenheimer, people like that. Hall: But his father worried about his career options, so he convinced James to try a biology course. Rothman: And I just fell in love. Hall: So, he ditched physics and decided to go to Harvard Medical School to learn more about biology. Rothman: In the end I never finished medical school. Hall: But, while he was there, he stumbled upon his life’s work. Rothman: I was a first-year medical student and I was listening to a lecture in our course on histology and cell biology. Hall: The professor was showing images that had been captured by scientists only a few decades before. They showed, for the first time, how complex the cell is. Rothman: The cell is not just, like a dumb little liquid inside. It's a highly organized place. It's more like a city than anything else. © 2023 Scientific American,

Keyword: Biomechanics
Link ID: 28805 - Posted: 05.31.2023

By Emily Underwood It’s a classic science fiction trope: Astronauts on an interstellar journey are kept in sleek, refrigerated pods in a state of suspended animation. Although such pods remain purely fictional, scientists have pursued research into inducing a hibernation-like state in humans to lessen the damage caused by medical conditions such as heart attacks and stroke, and to reduce the stress and costs of future long-distance space sojourns. In a study published today in Nature Metabolism, scientists report that they can trigger a similar state in mice by targeting part of their brain with pulses of ultrasound. Some experts are calling it a major technical step toward achieving this feat in humans, whereas others say it’s a stretch to extrapolate the results to our species. "It’s an amazing paper,” says Frank van Breukelen, a biologist who studies hibernation at the University of Nevada, Las Vegas and co-authored an editorial accompanying the study. The work builds on a flurry of recent studies that pinpoint specific populations of neurons in a region called the preoptic area (POA) of the hypothalamus. These cells act like an on-off switch for “torpor”—a sluggish, energy-saving state the animals enter when they’re dangerously cold or malnourished. In previous studies, scientists genetically engineered these neurons to respond to light or certain chemicals, and found they could cause mice to enter a torpid state even when they were warm and well-fed. Such invasive techniques can’t be easily translated to people, however, Breukelen notes. “That’s really not going to happen in people.” The new ultrasound study, led by bioengineer Hong Chen and her team at Washington University in St. Louis required no genetic engineering. Chen knew from previous research that some neurons have specialized pores called TRPM2 ion channels that change shape in response to ultrasonic waves, including the subset of POA cells that controls mouse torpor. To see what effect that had on the animals’ behavior, her team next glued miniature, speakerlike devices on the heads of mice to focus these waves on the POA.

Keyword: Sleep; Brain imaging
Link ID: 28800 - Posted: 05.27.2023

John Katsaras Charles Patrick Collier Dima Bolmatov Your brain is responsible for controlling most of your body’s activities. Its information processing capabilities are what allow you to learn, and it is the central repository of your memories. But how is memory formed, and where is it located in the brain? Although neuroscientists have identified different regions of the brain where memories are stored, such as the hippocampus in the middle of the brain, the neocortex in the top layer of the brain and the cerebellum at the base of the skull, they have yet to identify the specific molecular structures within those areas involved in memory and learning. Research from our team of biophysicists, physical chemists and materials scientists suggests that memory might be located in the membranes of neurons. Neurons are the fundamental working units of the brain. They are designed to transmit information to other cells, enabling the body to function. The junction between two neurons, called a synapse, and the chemistry that takes place between synapses, in the space called the synaptic cleft, are responsible for learning and memory. At a more fundamental level, the synapse is made of two membranes: one associated with the presynaptic neuron that transmits information, and one associated with the postsynaptic neuron that receives information. Each membrane is made up of a lipid bilayer containing proteins and other biomolecules. The changes taking place between these two membranes, commonly known as synaptic plasticity, are the primary mechanism for learning and memory. These include changes to the amounts of different proteins in the membranes, as well as the structure of the membranes themselves.

Keyword: Learning & Memory
Link ID: 28777 - Posted: 05.10.2023

By Geoffrey Giller From the brightly colored poison frogs of South America to the prehistoric-looking newts of the Western US, the world is filled with beautiful, deadly amphibians. Just a few milligrams of the newt’s tetrodotoxin can be fatal, and some of those frogs make the most potent poisons found in nature. In recent years, scientists have become increasingly interested in studying poisonous amphibians and are starting to unravel the mysteries they hold. How is it, for example, that the animals don’t poison themselves along with their would-be predators? And how exactly do the ones that ingest toxins in order to make themselves poisonous move those toxins from their stomachs to their skin? Even the source of the poison is sometimes unclear. While some amphibians get their toxins from their diet, and many poisonous organisms get theirs from symbiotic bacteria living on their skin, still others may or may not make the toxins themselves — which has led scientists to rethink some classic hypotheses. Over the long arc of evolution, animals have often turned to poisons as a means of defense. Unlike venoms — which are injected via fang, stinger, barb, or some other specialized structure for offensive or defensive purposes — poisons are generally defensive toxins a creature makes that must be ingested or absorbed before they take effect. Amphibians tend to store their poisons in or on their skin, presumably to increase the likelihood that a potential predator is deterred or incapacitated before it can eat or grievously wound them. Many of their most powerful toxins — like tetrodotoxin, epibatidine and the bufotoxins originally found in toads — are poisons that interfere with proteins in cells, or mimic key signaling molecules, thus disrupting normal function. © 2023 Annual Reviews

Keyword: Neurotoxins
Link ID: 28757 - Posted: 04.29.2023

By Jake Buehler Shimmering, gelatinous comb jellies wouldn’t appear to have much to hide. But their mostly see-through bodies cloak a nervous system unlike that of any other known animal, researchers report in the April 21 Science. In the nervous systems of everything from anemones to aardvarks, electrical impulses pass between nerve cells, allowing for signals to move from one cell to the next. But the ctenophores’ cobweb of neurons, called a nerve net, is missing these distinct connection spots, or synapses. Instead, the nerve net is fused together, with long, stringy neurons sharing a cell membrane, a new 3-D map of its structure shows. While the nerve net has been described before, no one had generated a high-resolution, detailed picture of it. It’s possible the bizarre tissue represents a second, independent evolutionary origin of a nervous system, say Pawel Burkhardt, a comparative neurobiologist at the University of Bergen in Norway, and colleagues. Superficially similar to jellyfish, ctenophores are often called comb jellies because they swim using rows of beating, hairlike combs. The enigmatic phylum is considered one of the earliest to branch off the animal tree of life. So ctenophores’ possession of a simple nervous system has been of particular interest to scientists interested in how such systems evolved. Previous genetics research had hinted at the strangeness of the ctenophore nervous system. For instance, a 2018 study couldn’t find a cell type in ctenophores with a genetic signature that corresponded to recognizable neurons, Burkhardt says. Burkhardt, along with neurobiologist Maike Kittelmann of Oxford Brookes University in England and colleagues, examined young sea walnuts (Mnemiopsis leidyi) using electron microscopes, compiling many images to reconstruct the entire net structure. Their 3-D map of a 1-day-old sea walnut revealed the funky synapse-free fusion between the five sprawling neurons that made up the tiny ctenophore’s net. © Society for Science & the Public 2000–2023.

Keyword: Evolution
Link ID: 28745 - Posted: 04.22.2023

Miryam Naddaf Virtual models representing the brains of people with epilepsy could help to enable more-effective treatments of the disease by showing neurosurgeons precisely which zones are responsible for seizures. The models, created using a computational system known as the Virtual Epileptic Patient (VEP), have been developed as part of the Human Brain Project (HBP), a ten-year European initiative focused on digital brain research. The approach is being tested in a clinical trial called EPINOV, to evaluate whether it improves the success rate of epilepsy surgery. “It’s an example of personalized medicine,” says Aswin Chari, a neurosurgeon at University College London. VEP uses “the patient’s own brain scans [and] the patient’s own brainwave-recording data to build a model and improve our understanding of where their seizures are coming from”. Life-changing surgery Epileptic seizures are brought on by abnormal brain activity, and around one-third of the 50 million people living with epilepsy worldwide do not respond to anti-seizure drugs. “For those people, surgery is a huge game changer,” says Chari. It aims to free patients from seizures by removing parts of the epileptogenic zone — the brain region that is thought to initiate seizures. To identify the epileptogenic zone, clinicians currently use scanning techniques such as magnetic resonance imaging (MRI) and electroencephalogram (EEG) to investigate brain activity. They also perform stereoelectroencephalography (SEEG), which involves placing up to 16 electrodes, each 7 centimetres long, through the skull to monitor the activity of specific areas for 1–2 weeks. © 2023 Springer Nature Limited

Keyword: Epilepsy; Brain imaging
Link ID: 28732 - Posted: 04.09.2023

By Nora Bradford For the first time, scientists have recorded brain waves from freely moving octopuses. The data reveal some unexpected patterns, though it’s too early to know how octopus brains control the animals’ behavior, researchers report February 23 in Current Biology. “Historically, it’s been so hard to do any recordings from octopuses, even if they’re sedated,” says neuroscientist Robyn Crook of San Francisco State University, who was not involved in the study. “Even when their arms are not moving, their whole body is very pliable,” making attaching recording equipment tricky. Octopuses also tend to be feisty and clever. That means they don’t usually put up with the uncomfortable equipment typically used to record brain waves in animals, says neuroethologist Tamar Gutnick of the University of Naples Federico II in Italy. To work around these obstacles, Gutnick and colleagues adapted portable data loggers typically used on birds, and surgically inserted the devices into three octopuses. The researchers also placed recording electrodes inside areas of the octopus brain that deal with learning and memory. The team then recorded the octopuses for 12 hours while the cephalopods went about their daily lives — sleeping, swimming and self-grooming — in tanks. Some brain wave patterns emerged across all three octopuses in the 12-hour period. For instance, some waves resembled activity in the human hippocampus, which plays a crucial role in memory consolidation. Other brain waves were similar to those controlling sleep-wake cycles in other animals. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28716 - Posted: 03.25.2023

Jon Hamilton Mora Leeb places some pieces into a puzzle during a local puzzle tournament. The 15-year-old has grown up without the left side of her brain after it was removed when she was very young. Seth Leeb In most people, speech and language live in the brain's left hemisphere. Mora Leeb is not most people. When she was 9 months old, surgeons removed the left side of her brain. Yet at 15, Mora plays soccer, tells jokes, gets her nails done, and, in many ways, lives the life of a typical teenager. "I can be described as a glass-half-full girl," she says, pronouncing each word carefully and without inflection. Her slow, cadence-free speech is one sign of a brain that has had to reorganize its language circuits. Yet to a remarkable degree, Mora's right hemisphere has taken on jobs usually done on the left side. It's an extreme version of brain plasticity, the process that allows a brain to modify its connections to adapt to new circumstances. Brain plasticity is thought to underlie learning, memory, and early childhood development. It's also how the brain revises its circuitry to help recover from a brain injury — or, in Mora's case, the loss of an entire hemisphere. Scientists hope that by understanding the brains of people like Mora, they can find ways to help others recover from a stroke or traumatic brain injury. They also hope to gain a better understanding of why very young brains are so plastic. Sometime in the third trimester of Ann Leeb's pregnancy, the child she was carrying had a massive stroke on the left side of her brain. No one knew it at the time. © 2023 npr

Keyword: Development of the Brain; Epilepsy
Link ID: 28714 - Posted: 03.23.2023

By Lisa Sanders, M.D. “It’s happening,” the 58-year-old man said quietly. Dr. Mark Chelmowski looked over to observe his patient. He was leaning forward, elbows on table, head propped up on his hands. Beads of sweat suddenly appeared on the man’s brow. More popped up on his cheeks, then his jaw. Rivulets ran down the contours of his face, then dripped off his chin onto the table. The man’s eyes were closed. He almost seemed asleep. Chelmowski said his name. “Yes, doctor” was the only response the normally chatty man gave. It was as if he were somehow distracted by the profound sweating. The patient’s vital signs were normal. He didn’t have a fever. His blood pressure and heart rate were normal. Throughout the exam, the patient sat quietly sweating. The collar, front and back of his shirt darkened. Then, as abruptly as it started, it was over. He opened his eyes and looked at Chelmowski. The patient could see the surprise in his doctor’s face. Chelmowski knew about his episodes of sweating — the two of them had been trying to figure them out for the past five months — but he had not yet witnessed one. The first time it happened, the patient was in his car on the way to the gym when suddenly he felt intensely hot. It was a bright July day in the Milwaukee area and seasonably warm. But this heat felt as if it came from inside his body. A vague prickling sensation spread down his face and neck to his chest and back. His heart seemed to speed up and then — pow — he was drenched in sweat. He turned the car around and headed home. He was describing the strange event to his partner when it happened again. And again. Each episode lasted only a couple of minutes, but it was strange. The sweating was so excessive. After a fourth episode, the patient’s partner insisted they go to the emergency room. He had another bout in front of the E.R. doctor, who immediately admitted him to the hospital. He was worried the patient might be having a heart attack. Profuse sweating often accompanies myocardial infarctions, the doctor told him. But it wasn’t his heart. He was discharged the next day and encouraged to follow up with his primary-care doctor. © 2023 The New York Times Company

Keyword: Epilepsy; Hormones & Behavior
Link ID: 28696 - Posted: 03.11.2023

by Laura Dattaro Neurons deep in the prefrontal cortex of fragile X model mice have trouble generating the electrical spikes needed to transmit information, according to a new study. The difficulty originates from faulty sodium channels. Fragile X syndrome, one of the leading genetic causes of autism, results from mutations in the gene FMR1. People with the condition often have difficulty with executive-function skills, such as working memory and planning. The new study may explain why, says Randi Hagerman, medical director of the MIND Institute at the University of California, Davis: The disruption to signals propagating through the prefrontal cortex may impede the region’s role in coordinating communication among other parts of the brain. Some drugs that regulate sodium channels, such as the diabetes drug metformin, are already approved for use in people. “This is a great animal model to look at the effects of medication,” says Hagerman, who was not involved in the new work. Mutations in the autism-linked gene SCN2A, which encodes a protein for the sodium channel Nav1.2, also suppress dendritic spikes, researchers previously showed in mice. The cellular mechanism for channel disruption is different between the models, but it’s possible that multiple genetic causes of autism “coalesce around sodium channel disfunction,” says Darrin Brager, research associate professor of neuroscience at the University of Texas at Austin and lead investigator on the FMR1 study. “The same channel is altered, and that’s changing the way the cells are able to integrate information and transmit it.” © 2023 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 28677 - Posted: 02.22.2023

Jon Hamilton When Tom's epileptic seizures could no longer be controlled with drugs, he started considering surgery. Tom – who asked that we not use his last name because he worries that employers might be alarmed by his medical history – was hoping doctors could remove the faulty brain tissue that sometimes caused him to convulse and lose consciousness. He underwent a grueling evaluation at the epilepsy center at the University of California, San Diego. Doctors removed a piece of his skull and placed electrodes on the surface of his brain. He spent a week in the hospital while doctors watched him having seizures. Then, he got bad news. "You're not an optimal surgery patient," he recalled the doctors telling him." We don't feel safe operating on you." That was in 2009. In 2018, with epilepsy taking a heavy toll on his work and family life, Tom went back to his doctors at UCSD to discuss treatment options. This time he met with Dr. Jerry Shih, the center's director. "I told him, you know what, we're in a unique situation now where we have some of the newer technologies that were not available" in 2009, Shih says. This time, the team inserted tiny electrodes into Tom's brain to find the primary source of his seizures. Then, in 2019, they used a laser to remove that bit of his brain. © 2023 npr

Keyword: Epilepsy
Link ID: 28665 - Posted: 02.15.2023

By Claudia López Lloreda Learning lots of new information as a baby requires a pool of ready-to-go, immature connections between nerve cells to form memories quickly. Called silent synapses, these connections are inactive until summoned to help create memories, and were thought to be present mainly in the developing brain and die off with time. But a new study reveals that there are many silent synapses in the adult mouse brain, researchers report November 30 in Nature. Neuroscientists have long puzzled over how the adult human brain can have stable, long-term memories, while at the same time maintaining a certain flexibility to be able to make new memories, a concept known as plasticity (SN: 7/27/12). These silent synapses may be part of the answer, says Jesper Sjöström, a neuroscientist at McGill University in Montreal who was not involved with the study. “The silent synapses are ready to hook up,” he says, possibly making it easier to store new memories as an adult by using these connections instead of having to override or destabilize mature synapses already connected to memories. “That means that there’s much more room for plasticity in the mature brain than we previously thought.” In a previous study, neuroscientist Mark Harnett of MIT and his colleagues had spotted many long, rod-shaped structures called filopodia in adult mouse brains. That surprised Harnett because these protrusions are mostly found on nerve cells in the developing brain. “Here they were in adult animals, and we could see them crystal clearly,” Harnett says. So he and his team decided to examine the filopodia to see what role they play, and if they were possibly silent synapses. The researchers used a technique to expand the brains of adult mice combined with high-resolution microscopy. Since nerve cell connections and the molecules called receptors that allow for communication between connected cells are so small, these methods revealed synapses that past research missed. © Society for Science & the Public 2000–2022.

Keyword: Learning & Memory
Link ID: 28602 - Posted: 12.17.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28580 - Posted: 12.03.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28579 - Posted: 12.03.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022

By Erika Check Hayden Weeks after Valeria Schenkel took an experimental drug named after her, the daily seizures that had afflicted her from birth became less frequent. But the drug caused fluid to build up in her brain, and a year later, she died at age 3. The drug was given to only one other child, and she experienced the same side effect and nearly died last year. The drug contained snippets of genetic material tailor-made to turn off the mutated gene causing the extremely rare form of epilepsy that these children were born with. A handful of researchers and nonprofit organizations have raised millions of dollars to make these treatments, known as antisense drugs, for at least 19 children and adults with severe diseases that are too rare to garner interest from pharmaceutical companies. The treatments have helped some of these patients, raising hopes that the personalized approach might one day save thousands of lives. But the brain side effect, known as hydrocephalus, reported on Sunday at the American Neurological Association meeting in Chicago, is a blow for the niche medical field that has made rapid progress over the past five years. Hydrocephalus happens when too much fluid fills cavities in the brain, increasing pressure on brain tissue and risking lethal damage if untreated. “I think it’s worth saying: No question that encountering hydrocephalus has been a setback, sobering and important,” said Dr. Timothy Yu, the neurologist and genetics researcher at Boston Children’s Hospital who developed the drug, known as valeriasen. But traditional drug companies, he added, are not helping patients with thousands of rare, untreatable and rapidly progressing diseases that cause death and severe disabilities. Personalized genetic treatments may be their only hope. “We have to learn as much as we can from each and every one, because they’re just so incredibly valuable in every sense,” Dr. Yu said. Scientists first imagined creating “antisense oligonucleotide” drugs — pieces of custom-made DNA or RNA designed to correct for genetic errors in cells — in the 1960s. But it took decades to make stable and effective versions of such drugs. © 2022 The New York Times Company

Keyword: Epilepsy; Development of the Brain
Link ID: 28529 - Posted: 10.28.2022

By Sandra G. Boodman For years Carter Caldwell had adamantly rejected doctors’ recommendations that he consider surgery to treat the frequent, uncontrolled seizures that were ravaging his brain. Caldwell, who had developed epilepsy when he was 28, regarded the operation that involved removing a portion of his brain as too big a risk — particularly because doctors weren’t sure what was causing the seizures and couldn’t pinpoint their location. Instead the Philadelphia business executive had organized his life to minimize certain foreseeable hazards: He lived downtown and didn’t drive. He didn’t push his toddler’s stroller. When taking the train he stood at the back of the platform — nowhere near the tracks in case he suddenly collapsed. His colleagues at work knew about his condition. But that calculus changed abruptly in November 2014. Caldwell, accompanied by his wife, Connie, and their 3-year-old son, was atop a hill at Pennsylvania’s Valley Forge National Historical Park posing for photos for a holiday card. Without warning he began an awkward shuffling walk that signified the onset of a seizure. Then he lost consciousness and fell head first down a rocky 15-foot embankment before landing at the edge of a stream. “Thankfully,” he said, “I didn’t roll into the stream.” He spent the next 2 1/2 weeks in a nearby hospital where a plastic surgeon performed multiple operations on his broken jawbone, lacerated cheek and shattered eye socket. “I remember him saying, ‘I can’t believe this happened in front of my family,’ ” recalled his longtime neurologist John R. Pollard, formerly associate director of the epilepsy center at the University of Pennsylvania. Pollard had warned Caldwell that his intractable seizures, which had proved resistant to numerous medications, placed him at risk for sudden death or serious injury. In September 2015 a successful operation unmasked the very unusual cause of Caldwell’s seizures, a culprit experts had long suspected but had been unable to definitively identify.

Keyword: Epilepsy; Emotions
Link ID: 28518 - Posted: 10.19.2022

By Lisa Sanders, M.D. “What just happened?” The 16-year-old girl’s voice was flat and tired. “I think you had a seizure,” her mother answered. Her daughter had asked to be taken to the pediatrician’s office because she hadn’t felt right for the past several weeks — not since she had what looked like a seizure at school. And now she’d had another. “You’re OK now,” the mother continued. “It’s good news because it means that maybe we finally figured out what’s going on.” To most people, that might have been a stretch — to call having a seizure good news. But for the past several years, the young woman had been plagued by headaches, episodes of dizziness and odd bouts of profound fatigue, and her mother embraced the possibility of a treatable disorder. The specialists she had taken her daughter to see attributed her collection of symptoms to the lingering effect of the many concussions she suffered playing sports. She had at least one concussion every year since she was in the fourth grade. Because of her frequent head injuries, her parents made her drop all her sports. Even when not on the playing field, the young woman continued to fall and hit her head. The headaches and other symptoms persisted long after each injury. She saw several specialists who agreed that she had what was called persistent post-concussive syndrome — symptoms caused either by a severe brain injury or, in her case, repeated mild injuries. She should get better with time and patience, the girl and her mother were told. And yet her head pounded and she retreated to her darkened room several times a week. She did everything her doctors suggested: She got plenty of sleep, rested when she was tired and tried to be patient. But she still got headaches, still got dizzy. She found it harder and harder to pay attention. For the past couple of years, it had even started to affect her grades. © 2022 The New York Times Company

Keyword: Epilepsy; Attention
Link ID: 28514 - Posted: 10.15.2022

James Brunton Badenoch Monkeypox’s effect on the skin – the disfiguring rashes – and the flu-like symptoms have been well described, but few have investigated the neurological and psychiatric problems the virus might cause. There are historic reports of neurological complications in people infected with the related smallpox virus and in people vaccinated against smallpox, which contains the related vaccinia virus. So my colleagues and I wanted to know whether monkeypox causes similar problems. We looked at all the evidence from before the current monkeypox pandemic of neurological or psychiatric problems in people with a monkeypox infection. The results are published in the journal eClinicalMedicine. A small but noticeable proportion of people (2% to 3%) with monkeypox became very unwell and developed serious neurological problems, including seizure and encephalitis (inflammation of the brain that can cause long-term disability). We also found that confusion occurred in a similar number of people. It’s important to note, though, that these figures are based on a few studies with few participants. Besides the severe and rare brain problems, we found evidence of a broader group of people with monkeypox who had more common neurological symptoms including headache, muscle ache and fatigue. From looking at the studies, it was unclear how severe these symptoms were and how long they lasted. It was also unclear how many people with monkeypox had psychiatric problems - such as anxiety and depression - as few studies looked into it. Of those that did, low mood was frequently reported.. © 2010–2022, The Conversation US, Inc.

Keyword: Epilepsy; Learning & Memory
Link ID: 28475 - Posted: 09.14.2022