By Benjamin Mueller It appeared to be an ordinary fall: Bob Saget, the actor and comedian, knocked his head on something and, perhaps thinking nothing of it, went to sleep, his family said on Wednesday. But the chilling consequences — Mr. Saget, 65, died some hours later on Jan. 9 from blunt head trauma, a medical examiner ruled — have underscored the dangers of traumatic brain injuries, even those that do not initially seem to be causes for alarm. Some 61,000 deaths in 2019 were related to traumatic brain injuries, according to the Centers for Disease Control and Prevention, and nearly half of head trauma-related hospitalizations result from falls. Brain injury experts said on Thursday that Mr. Saget’s case was relatively uncommon: People with serious head trauma would be expected to have noticeable symptoms, like a headache, nausea or confusion. And they can generally be saved by surgeons opening up their skull and relieving pressure on the brain from bleeding. But certain situations put people at higher risk for the sort of deterioration that Mr. Saget experienced, doctors said. As serious a risk factor as any, doctors said, is simply being alone. Someone with a head injury can lose touch with their usual decision-making capacities and become confused, agitated or unusually sleepy. Those symptoms, in turn, can stand in the way of getting help. And while there was no indication that Mr. Saget was taking blood thinners, experts said the medications can greatly accelerate the type of bleeding after a head injury that forces the brain downward and compresses the centers that regulate breathing and other vital functions. More Americans are being prescribed these drugs as the population ages. Mr. Saget had been in an Orlando hotel room during a weekend of stand-up comedy acts when he was found unresponsive. The local medical examiner’s office announced on Wednesday that his death resulted from “blunt head trauma,” and said that “his injuries were most likely incurred from an unwitnessed fall.” © 2022 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 28201 - Posted: 02.12.2022

ByKelly Servick In 1997, Laura Gould put her 15-month-old daughter, Maria, down for a nap and returned to find her unresponsive. She had died suddenly, with no clues to explain the tragedy besides a fever the night before. When her daughter’s body was sent to the medical examiner’s office, “I thought they’d call me in an hour and tell me what happened … like on TV,” Gould says. Months later, neither that office nor independent pathologists had an explanation. “I hated ending it with ‘the autopsy was inconclusive, go on and live your life now,’” she says. “It just didn’t really feel like that was an option.” Gould co-founded a nonprofit foundation to support grieving parents, raise research funds, and increase awareness of sudden unexplained death in childhood (SUDC), a term used for children older than 12 months. In the United States, roughly 400 deaths fall into this category each year—about one-quarter as many as are labeled sudden infant death syndrome (SIDS). Two recent genetic analyses, one funded in part by Gould’s SUDC Foundation, now suggest potential causes for at least a small fraction of cases: mutations in genes associated with epilepsy, heart arrhythmias, and neurodevelopmental disorders. “Having this data is important,” says Marco Hefti, a neuropathologist at the University of Iowa Carver College of Medicine who was not involved in the new studies. SUDC is not a single disease, but “a grab bag of different things—and the more of those different things you can pull out, the better for everybody.” Neither study can say with certainty that a mutation is responsible for a child’s death. But the findings provide a basis for animal studies that could reveal how the genetic changes interfere with vital functions. They might also inform future child death investigations and potentially even screening programs to prevent deaths. Research on SUDC has lagged that on the more common and better known SIDS. Yet, biologically, SIDS and SUDC “may be part of a spectrum,” says Ingrid Holm, a medical geneticist at Boston Children’s Hospital. In both, death often occurs during sleep, and researchers suspect contributors including undetected heart defects, metabolic disorders, and central nervous system abnormalities. The children who die are roughly 10 times more likely than the average child to have a history of febrile seizures—convulsions that come with fevers in young children, notes neurologist Orrin Devinsky of New York University (NYU) Langone Health. © 2022 American Association for the Advancement of Science.

Keyword: Sleep; Genes & Behavior
Link ID: 28200 - Posted: 02.12.2022

Natalia Mesa More than a decade ago, scientists developed optogenetics, a method to turn cells on and off with light. The technique allows scientists to spur or suppress cells' electrical activity with just the flip of a switch to tease apart the roles of specific cell types. But because light doesn’t penetrate deep into tissues, scientists need to surgically implant light sources to illuminate cells below the surface of the skin or skull. In a new study published today (February 9) in Nature Communications, researchers report they’ve found a way to use ultrasound to noninvasively activate mouse neurons, both in culture and in the brains of living animals. The technique, which the authors call sonogenetics, elicits electrical activity in a subset of brain cells that have been genetically engineered to respond to sound waves. “We know that ultrasound is safe,” study coauthor Sreekanth Chalasani, a neuroscientist in Salk’s Molecular Neurobiology Laboratory, tells The Scientist. “The potential for neuronal control is huge. It has applications for pacemakers, insulin pumps, and other therapies that we’re not even thinking about. Jamie Tyler, a biomedical engineer at the University of Alabama at Birmingham who was not involved in the study but has previously collaborated with some of its authors, tells The Scientist that the work represents “more than just a step forward” in being able to use ultrasound to control neural activity: “It shows that sonogenetics is a viable technique in mammalian cells.” © 1986–2022 The Scientist.

Keyword: Brain imaging
Link ID: 28199 - Posted: 02.12.2022

ByTess Joosse Bite into a lemon and you’ll likely experience a clashing rush of sensations: crushing sharpness, mouth-watering tanginess, and pleasant brightness. But despite its assertiveness—and its role as one of the five main taste profiles (along with sweet, salty, savory, and bitter)—scientists don’t know much about how our acidic taste evolved. Enter Rob Dunn. The North Carolina State University ecologist and his collaborators have spent years scanning the scientific literature in search of an answer. In a paper published this week in the Proceedings of the Royal Society B, the team reports some clues. Science chatted with Dunn about how, and why, humans like to pucker up. This interview has been edited for clarity and length. Rob Dunn Ecologist Rob DunnAmanda Ward Q: Do other animals like sour foods? A: With almost all the other tastes, species have lost them through evolution. Dolphins appear to have no taste receptors other than salty, and cats don’t have sweet taste receptors. That’s what we expected to see with sour. What we see instead is all the species that have been tested [about 60 so far] are able to detect acidity in their food. Of those animals, pigs and primates seem to really like acidic foods. For example, wild pigs (Sus scrofa) are really attracted to fermented corn, and gorillas (Gorilla gorilla) have shown a preference for acidic fruits in the ginger family. Q: Sweet taste gives us a reward for energy, and bitter alerts us to potential poisons. Why might we have evolved a taste for sour? A: Sour taste was likely present in ancient fish—they’re the earliest vertebrate animals that we know can sense sour. The origin in fish was likely not to taste food with their mouths, but to sense acidity in the ocean—basically fish “tasting” with the outside of their body. Variations in dissolved carbon dioxide can create acidity gradients in the water, which can be dangerous for fish. Being able to sense acidity would have been important. © 2022 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 28198 - Posted: 02.12.2022

Ian Sample Science editor People who develop Alzheimer’s disease can experience sleep disturbances years before the condition takes hold, but whether one causes the other, or something more complex is afoot, has always proved hard for scientists to determine. Now, researchers in the US have shed light on the mystery, in work that raises hopes for new therapies, and how “good sleep hygiene” could help to tackle the disease and its symptoms. The findings show that humans’ 24-hour circadian clock controls the brain’s ability to mop up wayward proteins linked to Alzheimer’s disease. If the scientists are right, the work would explain, at least in part, how disruption to circadian rhythms and sleep disturbances might feed into the onset and progression of Alzheimer’s disease, and how preventing such disruption might stave off the condition. “Circadian disruption is correlated with Alzheimer’s diagnosis and it has been suggested that sleep disruptions could be an early warning sign of Alzheimer’s disease,” said Dr Jennifer Hurley, who led the research at Rensselaer Polytechnic Institute, in New York. Alzheimer’s takes hold when connections are lost between nerve cells in the brain. The disease is progressive and linked to abnormal plaques and tangles of proteins that steadily build up in the brain. The disease is the most common cause of dementia and affects more than half a million people in the UK, a figure that is set to rise. To keep the brain healthy, immune cells called microglia seek out and destroy troublesome proteins that threaten to accumulate in the brain. One type of protein targeted by the cells is called amyloid beta, a hallmark of Alzheimer’s. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Sleep
Link ID: 28197 - Posted: 02.12.2022

By Elizabeth Landau My grandmother was in the advanced stages of Alzheimer’s disease when she died in 2007, not long after I graduated from journalism school. As a budding health reporter, I tried to learn everything I could about Alzheimer’s and wrote about new research on preventions and treatments that everyone wanted to believe had potential. It is demoralizing and infuriating to think about how, nearly 15 years later, no breakthrough cure or proven prevention strategy has panned out. But neurologist Sara Manning Peskin argues in “A Molecule Away from Madness: Tales of the Hijacked Brain” that we could be on the brink of a revolution in confronting diseases like this because scientists have a better handle on how molecules work in the brain. Molecular research has transformed our understanding and treatment of cancer in recent years, and now it is beginning to do the same for brain diseases. In fact, it has already been key to solving several mysteries of why seemingly healthy people appear to suddenly fall into a mental inferno. While the shadow of Alzheimer’s looms over the book, representing an intractable condition that Peskin routinely confronts in her clinical practice, “A Molecule Away from Madness” is a fascinating tour of different kinds of ways that the brain can lead to the breakdown of mental life. The book is organized according to how different molecules interact with our brains to wreak havoc — Peskin calls them “mutants, rebels, invaders, and evaders.” Some have helped scientists solve longstanding puzzles, while others, like the molecules associated with Alzheimer’s, continue to leave millions of people waiting for a cure.

Keyword: Alzheimers
Link ID: 28196 - Posted: 02.12.2022

By Lenny Bernstein The federal government on Thursday proposed new guidelines for prescribing opioids that would eliminate numerical dosage recommendations for treatment of chronic pain in favor of a more flexible approach by caregivers. FAQ: What to know about the omicron variant of the coronavirus The recommendations call for doctors and other prescribers to weigh the risks and benefits of starting, increasing and halting treatment with opioids. They leave out previous advice on the amount and duration of painkiller treatments that patients and doctors have contended was sometimes misinterpreted, causing serious harm to people suffering unrelenting pain. For some with chronic pain, the problem is not in their backs or knees but their brains Some states and caregivers adopted tight rules based on the recommendations, first issued in 2016, resulting in patients having difficulty obtaining pain drugs or having them cut off abruptly. “There’s not a one size fits all,” said Christopher Jones, acting director of the National Center for Injury Prevention and Control, part of the Centers for Disease Control and Prevention. “We’ve heard that quite clearly. When you have hard thresholds like 90 [morphine milligram equivalents] or a specific duration, it makes it too easy for policymakers or others to take that out of context and apply that as a rigid cap.” Bobby Mukkamala, chairman of the American Medical Association Board of Trustees, issued a statement saying that “for nearly six years, the AMA has urged the CDC to reconsider its problematic guideline on opioid prescriptions that proved devastating for patients with pain. The CDC’s new draft guideline — if followed by policymakers, health insurance companies and pharmacy chains — provides a path to remove arbitrary prescribing thresholds, restore balance and support comprehensive, compassionate care.” Andrew Kolodny, one of the fiercest critics of opioid manufacturers, said he believes some of the opposition was orchestrated by drug companies that saw the attempt to curb opioid prescribing — especially of high-dose pills — as a threat to their profit margins. © 1996-2022 The Washington Post

Keyword: Drug Abuse
Link ID: 28195 - Posted: 02.12.2022

By Pallab Ghosh A paralysed man with a severed spinal cord has been able to walk again, thanks to an implant developed by a team of Swiss researchers. It is the first time someone who has had a complete cut to their spinal cord has been able to walk freely. The same technology has improved the health of another paralysed patient to the extent that he has been able to become a father. The research has been published in the journal Nature Medicine. Michel Roccati was paralysed after a motorbike accident five years ago. His spinal cord was completely severed - and he has no feeling at all in his legs. But he can now walk - because of an electrical implant that has been surgically attached to his spine. Someone this injured has never been able to walk like this before. The researchers stress that it isn't a cure for spinal injury and that the technology is still too complicated to be used in everyday life, but hail it nonetheless as a major step to improving quality of life. I met Michel at the lab where the implant was created. He told me that the technology "is a gift to me". "I stand up, walk where I want to, I can walk the stairs - it's almost a normal life." It was not the technology alone that drove Michel's recovery. The young Italian has a steely resolve. He told me that from the moment of his accident, he was determined to make as much progress as he could. "I used to box, run and do fitness training in the gym. But after the accident, I could not do the things that I loved to do, but I did not let my mood go down. I never stopped my rehabilitation. I wanted to solve this problem." The speed of Michel's recovery amazed the neurosurgeon who inserted the implant and expertly attached electrodes to individual nerve fibres, Prof Jocelyne Bloch at Lausanne University Hospital "I was extremely surprised," she told me. "Michel is absolutely incredible. He should be able to use this technology to progress and be better and better." © 2022 BBC.

Keyword: Robotics; Regeneration
Link ID: 28194 - Posted: 02.09.2022

Jon Hamilton Paul knew his young grandson was in danger. "Out of the corner of my eye I could see this little figure moving," he says. The figure was heading for a steep flight of stairs. But what could he do? Paul was sitting down. And after more than a decade of living with Parkinson's disease, getting out of a chair had become a long and arduous process. But not on this day. "Paul jumped up from the chair and ran to my grandson," says his wife, Rose. (The couple asked to be identified by only their first names to protect their medical privacy.) "I mean, he just got up like there was nothing and ran to pick up Max." Amazing. But it's also the kind of story that's become familiar to Peter Strick, professor and chair of neurobiology at the University of Pittsburgh and scientific director of the University of Pittsburgh Brain Institute. "It was a great example of what people call paradoxical kinesia," Strick says. "It was a description of just what we are studying." Article continues after sponsor message Paradoxical kinesia refers to the sudden ability of a person with Parkinson's to move quickly and fluidly, the way they did before the disease eroded a brain area involved in movement. The phenomenon is a variation of the placebo effect. But instead of being induced by the belief that a sugar pill is really medicine, it tends to appear in situations that involve stress or a strong emotion. For Paul, "it was the fear of his grandson falling down the stairs," says Strick, who learned about the event in an email from Rose. A treatment that's "all in your head" © 2022 npr

Keyword: Parkinsons; Emotions
Link ID: 28193 - Posted: 02.09.2022

By Christina Caron After 10 years of marriage, Ree, 42, and her husband were ready to call it quits. Even their therapist had given up, she said, in part because her husband “was so closed off, just unable to open up.” “We loved each other a lot and we were very compatible, however, we didn’t know how to deal with conflict,” Ree said. She was often anxious about their relationship and could be “a little neurotic at times,” but the more she pushed her husband to connect, the more withdrawn he became. Their sex life suffered. Then a friend suggested that they try the illegal drug MDMA, popularly known as Ecstasy or Molly. For Ree — who, along with her husband, requested anonymity to speak about drug use, and is referred to by a nickname — the answer was an “immediate no.” MDMA, long associated with rave culture, is currently categorized as a Schedule I drug — meaning it has a high potential for abuse and no accepted medical use in the United States. “We are about as strait-laced as you can come,” she said. “We’re not people who break laws or do drugs.” Six months later, after reading “How to Change Your Mind,” the best-selling book by Michael Pollan that details his transformative experience with psychedelics, Ree reconsidered. And that’s how they found themselves in a secluded area of Utah at a large, rented house with a beautiful view of the mountains to trip on MDMA with five other couples. In recent years, clinical trials have shown that MDMA, when combined with talk therapy, can bring relief to those suffering from post-traumatic stress disorder, a finding that has elevated MDMA’s reputation from party drug to potential therapeutic. Some couples, drawn to the drug’s ability to produce feelings of empathy, trust and compassion, have started using unregulated MDMA on their own in an effort to help them reconnect, improve communication and have better sex. © 2022 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 28192 - Posted: 02.09.2022

Ian Sample Science editor Getting an hour or so more sleep each night can help people to cut calories, according a small clinical trial in overweight adults. Researchers in the US found that people who typically slept for less than 6.5 hours a night shed an average of 270 calories from their daily intake when they got an extra 1.2 hours of sleep. Sustained over three years, the reduction in calories could lead people to lose about 12kg (26lbs) without changing their diet during the day, the scientists believe. Some participants in the study consumed 500 fewer calories a day after improving their sleep. The study was not designed to look at weight loss, but researchers noticed the fall in calories within two weeks of patients changing their sleep patterns. “If healthy sleep habits are maintained over longer duration, this would lead to clinically important weight loss over time,” said Dr Esra Tasali, of the University of Chicago’s sleep centre. “Many people are working hard to find ways to decrease their caloric intake to lose weight – well, just by sleeping more, you may be able to reduce it substantially.” The trial studied 80 adults aged 21 to 40 with a body mass index between 25 and 29.9, meaning they were overweight. Half of the participants were randomly assigned to receive personalised sleep hygiene counselling aimed at extending the amount of time they slept each night. © 2022 Guardian News & Media Limited

Keyword: Sleep; Obesity
Link ID: 28191 - Posted: 02.09.2022

By Hallie Levine If you have ever had a ringing or buzzing in one or both ears after a live concert, you have experienced tinnitus — defined as the perception of noise where no external noise is present, according to the American Tinnitus Association. Aside from loud sound, a variety of issues, like excess ear wax, infections and nasal congestion, can cause short-term tinnitus. After a loud event like a concert, the intrusive sounds usually fade within hours to days. But chronic tinnitus — where noise persistently waxes and wanes, or never disappears — affects about 11 percent of adults. In some cases, this can lead to trouble sleeping or concentrating, isolation, anxiety, depression and stress. A 2019 research letter published in JAMA Otolaryngology Head & Neck Surgery found that women with undiagnosed tinnitus were even at increased risk of suicide. Is there a covid-19 connection? During the pandemic, reports of tinnitus rose, especially in people with covid-19. A study published online last March in the International Journal of Audiology estimated that almost 15 percent of those with covid-19 said they had tinnitus, often early in the course of the virus. This typically lasted only a few days. But “there have been anecdotal reports from patients that they have experienced changes in hearing and tinnitus post-covid,” says Cleveland Clinic audiologist Sarah Sydlowski, president of the American Academy of Audiology. One theory is that the virus that causes covid-19 damages the auditory nerve at least temporarily, says Douglas Hildrew, an ear, nose, and throat (ENT) specialist at Yale Medicine.

Keyword: Hearing
Link ID: 28190 - Posted: 02.09.2022

By Laura Sanders A tussle with COVID-19 can leave people’s brains fuzzy. SARS-CoV-2, the virus behind COVID-19, doesn’t usually make it into the brain directly. But the immune system’s response to even mild cases can affect the brain, new preliminary studies suggest. These reverberating effects may lead to fatigue, trouble thinking, difficulty remembering and even pain, months after the infection is gone. It’s not a new idea. Immune systems gone awry have been implicated in cognitive problems that come with other viral infections such as HIV and influenza, with disorders such as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, and even from the damaging effects of chemotherapy. What’s different with COVID-19 is the scope of the problem. Millions of people have been infected, says neurologist Avindra Nath of the National Institutes of Health in Bethesda, Md. “We are now faced with a public health crisis,” he says. Sign up for e-mail updates on the latest coronavirus news and research To figure out ways to treat people for the fuzzy thinking, headaches and fatigue that hang around after a bout with COVID-19, scientists are racing to figure out what’s causing these symptoms (SN: 4/27/21). Cognitive neurologist Joanna Hellmuth at the University of California, San Francisco had a head start. As someone who had studied the effects of HIV on the brain, she quickly noted similarities in the neurological symptoms of HIV and COVID-19. The infections paint “the same exact clinical picture,” she says. HIV-related cognitive symptoms have been linked to immune activation in the body, including the brain. “Maybe the same thing is happening in COVID,” Hellmuth says. © Society for Science & the Public 2000–2022.

Keyword: Neuroimmunology; Learning & Memory
Link ID: 28189 - Posted: 02.05.2022

ByElizabeth Pennisi The trillions of bacteria in and on our bodies can bolster our health and contribute to disease, but just which microbes are the key actors has been elusive. Now, a study involving thousands of people in Finland has identified a potential microbial culprit in some cases of depression. The finding, which emerged from a study of how genetics and diet affect the microbiome, “is really solid proof that this association could have major clinical importance,” says Jack Gilbert, a microbial ecologist at the University of California, San Diego, who was not involved with the work. Researchers are finding ever more links between brain conditions and gut microbes. People with autism and mood disorders, for example, have deficits of certain key bacteria in their guts. Whether those microbial deficits actually help cause the disorders is unclear, but the findings have spawned a rush to harness gut microbes and the substances they produce as possible treatments for a variety of brain disorders. Indeed, researchers recently reported in Frontiers in Psychiatry that fecal transplants improved symptoms in two depressed patients. Guillaume Méric didn’t set out to find microbes that cause depression. A microbial bioinformatician at the Baker Heart & Diabetes Institute, he and his colleagues were analyzing data from a large health and lifestyle study from Finland. Part of a 40-year effort to track down underlying causes of chronic disease in Finnish people, the 2002 study assessed the genetic makeup of 6000 participants, identified their gut microbes, and compiled extensive data about their diets, lifestyles, prescription drug use, and health. Researchers tracked the health of participants until 2018. Méric and his colleagues combed the data for clues to how a person’s diet and genetics affect the microbiome. “There have been very few studies that have examined [all these factors] in such detail,” Gilbert says. Two sections of the human genome seemed to strongly influence which microbes are present in the gut, the researchers report this week in Nature Genetics. One contains the gene for digesting the milk sugar lactose, and the other helps specify blood type. (A second study, also published today in Nature Genetics, identified the same genetic loci by analyzing the relationship between the genomes and gut microbes of 7700 people in the Netherlands.) © 2022 American Association for the Advancement of Science.

Keyword: Depression; Obesity
Link ID: 28188 - Posted: 02.05.2022

Anastasia Brodovskaya Jaideep Kapur Epilepsy is a disease marked by recurrent seizures, or sudden periods of abnormal, excessive or synchronous neuronal activity in the brain. One in 26 people in the U.S. will develop epilepsy at some point in their life. While people with mild seizures might experience a brief loss of awareness and muscle twitches, more severe seizures could last for several minutes and lead to injury from falling down and losing control of their limbs. Many people with epilepsy also experience memory problems. Patients often experience retrograde amnesia, where they cannot remember what happened immediately before their seizure. Electroconvulsive therapy, a form of treatment for major depression that intentionally triggers small seizures, can also cause retrograde amnesia. So why do seizures often cause memory loss? We are neurology researchers who study the mechanisms behind how seizures affect the brain. Our brain-mapping study found that seizures affect the same circuits of the brain responsible for memory formation. Understand new developments in science, health and technology, each week One of the earliest descriptions of seizures was written on a Babylonian tablet over 3,000 years ago. Seizures can be caused by a number of factors, ranging from abnormalities in brain structure and genetic mutations to infections and autoimmune conditions. Often, the root cause of a seizure isn’t known. The most common type of epilepsy involves seizures that originate in the brain region located behind the ears, the temporal lobe. Some patients with temporal lobe epilepsy experience retrograde amnesia and are unable to recall events immediately before their seizure. © 2010–2022, The Conversation US, Inc.

Keyword: Epilepsy; Learning & Memory
Link ID: 28187 - Posted: 02.05.2022

by Holly Barker New software uses machine-learning to automatically detect and quantify gait and posture from videos of mice moving around their cage. The tool could accelerate research on how autism-linked mutations or drug treatments affect motor skills, says lead researcher Vivek Kumar, associate professor of mammalian genetics at The Jackson Laboratory in Bar Harbor, Maine. Most efforts to analyze motor behavior involve placing a mouse on a treadmill or training it to walk through a maze. These assays are a simple way of testing speed, but they restrict the animals’ movement and force mice to walk in an unnatural way. The algorithm processes footage from an overhead camera and tracks 12 key points on a mouse’s body as it freely explores its surroundings. As the animal wanders, the software detects the position of its limbs and other body parts, automatically generating data on its gait and posture. The researchers described their method in January in Cell Reports. Kumar’s group trained the software by feeding it about 8,000 video frames that had been manually annotated to tag key points on the animal’s body, such as the nose, ears and tip of the tail. They repeated the process with a variety of different strains to teach the algorithm to recognize mice of all shapes and sizes. The trained software learned to read the rodent’s pose, which was further analyzed to extract more detailed information, such as the speed and length of each stride and the width of the mouse’s stance. © 2022 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 28186 - Posted: 02.05.2022

ByRodrigo Pérez Ortega A good workout doesn’t just boost your mood—it also boosts the brain’s ability to create new neurons. But exactly how this happens has puzzled researchers for years. “It’s been a bit of a black box,” says Tara Walker, a neuroscientist at the University of Queensland’s Brain Institute. Now, Walker and her colleagues think they have found a key: the chemical element selenium. During exercise, mice produce a protein containing selenium that helps their brains grow new neurons, the team reports today. Scientists may also be able to harness the element to help reverse cognitive decline due to old age and brain injury, the authors say. It’s a “fantastic” study, says Bárbara Cardoso, a nutritional biochemist at Monash University’s Victorian Heart Institute. Her own research has shown selenium—which is found in Brazil nuts, grains, and some legumes—improves verbal fluency and the ability to copy drawings correctly in older adults. “We could start thinking about selenium as a strategy” to treat or prevent cognitive decline in those who cannot exercise or are more vulnerable to selenium deficiency, she says, such as older adults, and stroke and Alzheimer’s disease patients. In 1999, researchers reported that running stimulates the brain to make new neurons in the hippocampus, a region involved in learning and memory. But which molecules were released into the bloodstream to spark this “neurogenesis” remained unclear. So 7 years ago, Walker and her colleagues screened the blood plasma of mice that had exercised on a running wheel in their cages for 4 days, versus mice that had no wheel. The team identified 38 proteins whose levels increased after the workout. © 2022 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 28185 - Posted: 02.05.2022

Bret Stetka It all started with genetic data. A gene here, a gene there. Eventually the story became clearer: If scientists are to one day find a cure for Alzheimer's disease, they should look to the immune system. Over the past couple decades, researchers have identified numerous genes involved in various immune system functions that may also contribute to Alzheimer's. Some of the prime suspects are genes that control humble little immune cells called microglia, now the focus of intense research in developing new Alzheimer's drugs. Microglia are amoeba-like cells that scour the brain for injuries and invaders. They help clear dead or impaired brain cells and literally gobble up invading microbes. Without them, we'd be in trouble. In a normal brain, a protein called beta-amyloid is cleared away through our lymphatic system by microglia as molecular junk. But sometimes it builds up. Certain gene mutations are one culprit in this toxic accumulation. Traumatic brain injury is another, and, perhaps, impaired microglial function. One thing everyone agrees on is that in people with Alzheimer's, too much amyloid accumulates between their brain cells and in the vessels that supply the brain with blood. Once amyloid begins to clog networks of neurons, it triggers the accumulation of another protein, called tau, inside of these brain cells. The presence of tau sends microglia and other immune mechanisms into overdrive, resulting in the inflammatory immune response that many experts believe ultimately saps brain vitality in Alzheimer's. To date, nearly a dozen genes involved in immune and microglial function have been tied to Alzheimer's. The first was CD33, identified in 2008. © 2022 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 28184 - Posted: 02.02.2022

By Amelia Nierenberg A couple of glasses of wine or a few drinks in the evening will probably make you fall asleep faster than normal. Who among us hasn’t left the dishes for the next morning or neglected a skin-care routine after a dinner party or festive night out? But even if you thud into dreamland, there’s a good chance that too much alcohol will mean a fitful night of sleep. That’s because alcohol disrupts what’s known as your sleep architecture, the normal phases of deeper and lighter sleep we go through every night. A night of drinking can “fragment,” or interrupt, these patterns, experts say, and you may wake up several times as you ricochet through the usual stages of sleep. “You pay for it in the second half of the night,” said Dr. Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles. Alcohol is “initially sedating, but as it’s metabolized, it’s very activating.” Here’s how it breaks down. In the first half of the night, when fairly high levels of alcohol are still coursing through your bloodstream, you’ll probably sleep deeply and dreamlessly. One reason: In the brain, alcohol acts on gamma-aminobutyric acid, or GABA, a neurotransmitter that inhibits impulses between nerve cells and has a calming effect. Alcohol can also suppress rapid eye movement, or REM sleep, which is when most dreaming occurs. Later in the night, as alcohol levels drop, your brain kicks into overdrive. You may toss and turn as your body undergoes a rebound arousal. “As the levels decline, you’re going to get more issues with the fragmentation,” said Dr. R. Nisha Aurora, a member of the board of directors of the American Academy of Sleep Medicine. You’ll also probably have more vivid or stressful dreams and — because fitful sleep means that you’re waking up more regularly — you are more likely to remember them.

Keyword: Sleep; Drug Abuse
Link ID: 28183 - Posted: 02.02.2022

Dan Robitzski As the coronavirus pandemic continues, scientists are racing to understand the underlying causes and implications of long COVID, the umbrella term for symptoms that persist for at least 12 weeks but often last even longer and affect roughly 30 percent of individuals who contract COVID-19. Evidence for specific risk factors such as diabetes and the presence of autoantibodies is starting to emerge, but throughout the pandemic, one assumption has been that an important indicator of whether a COVID-19 survivor is likely to develop long COVID is the severity of their acute illness. However, a preprint shared online on January 10 suggests that even mild SARS-CoV-2 infections may lead to long-term neurological symptoms associated with long COVID such as cognitive impairment and difficulties with attention and memory, a suite of symptoms often lumped together as “brain fog.” In the study, which has not yet been peer-reviewed, scientists led by Stanford University neurologist Michelle Monje identified a pathway in COVID-19–infected mice and humans that almost perfectly matches the inflammation thought to cause chemotherapy-related cognitive impairment (CRCI), also known as “chemo fog,” following cancer treatments. On top of that, the preprint shows that the neuroinflammation pathway can be triggered even without the coronavirus infecting a single brain cell. As far back as March 2020, Monje feared that cytokine storms caused by the immune response to SARS-CoV-2 would cause the same neuroinflammation and symptoms associated with CRCI, she tells The Scientist. But because her lab doesn’t study viral infections, she had no way to test her hypothesis until other researchers created the appropriate models. In the study, Monje and her colleagues used a mouse model for mild SARS-CoV-2 infections developed at the lab of Yale School of Medicine biologist and study coauthor Akiko Iwasaki as well as brain tissue samples taken from people who had COVID-19 when they died to demonstrate that mild infections can trigger inflammation in the brain. © 1986–2022 The Scientist.

Keyword: Learning & Memory
Link ID: 28182 - Posted: 02.02.2022