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By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

Keyword: Depression; Drug Abuse
Link ID: 28099 - Posted: 12.04.2021

By Pam Belluck AURORA, Ill. — There is sobering evidence of Samantha Lewis’s struggle with long Covid on her bathroom mirror. Above the sink, she has posted a neon pink index card scrawled with nine steps (4. Wet brush 5. Toothpaste) reminding her how to brush and floss her teeth. It is one of many strategies Ms. Lewis, 34, has learned from “cognitive rehab,” an intensive therapy program for Covid-19 survivors whose lives have been upended by problems like brain fog, memory lapses, dizziness and debilitating fatigue. Nearly two years into the pandemic, advances have been made in treating Covid itself, but long Covid — a constellation of lingering health problems that some patients experience — remains little understood. Post-Covid clinics around the country are trying different approaches to help patients desperate for answers, but there is little data on outcomes so far, and doctors say it is too soon to know what might work, and for which patients. While some physical symptoms of long Covid, like shortness of breath or nausea, can be addressed with medication, cognitive issues are more challenging. Few drugs exist, and while some deficits can rebound with time, they can also be exacerbated by resuming activities too soon or intensively. Over several months, The New York Times visited Ms. Lewis, interviewed her doctors, attended her therapy sessions and read her medical records. Before she was infected with the coronavirus in October 2020, experiencing a modest initial illness that did not require hospitalization, she was successfully juggling a demanding, detail-oriented job while raising a child with autism and attention deficit hyperactivity disorder. But this summer, she scored 25 on a 30-point assessment, placing her in a pre-dementia category called mild cognitive impairment. © 2021 The New York Times Company

Keyword: Learning & Memory
Link ID: 28098 - Posted: 12.04.2021

By Bob Goldstein On a cold, dry Tuesday in December, 1940, Rita Levi-Montalcini rode a train from the station near her home in Turin, Italy, for 80 miles to Milan to buy a microscope. Milan had not seen bombings for months. On her return to the Turin train station, two police officers stopped her and demanded to see inside the cake-sized box that she was carrying. With wartime food rationing, panettone cakes were only available illegally. The officers found her new microscope instead. They let her go. Just a week after her trip, British bombers hit Milan. Levi-Montalcini was a 31-year-old scientist who had been working at the University of Turin. Despite her father’s disapproval, she had trained in medicine, inspired by seeing a nanny succumb to cancer. In 1938, the Italian dictator Mussolini banned Jews from positions in universities. Levi-Montalcini was not raised in the Jewish religion, but her Jewish ancestry would have been evident from her surname. Mussolini’s ban had pushed Levi-Montalcini to leave Italy for Belgium in 1939, where she did research using fertilized chicken eggs as a source of material for her research topic: the developing nervous systems of vertebrate embryos. Levi-Montalcini also spent time with her older sister Nina, whose family was in Belgium as well. Rita wrote home to her mother of an “infinite desire to embrace you again,” but research at the university in Turin would have been impossible had she returned home. Her passion for research alternated with her frustration with challenges. When Hitler invaded Poland in September, launching war, her worst frustrations were realized. The “whole world was in danger,” Levi-Montalcini later wrote. In December 1939, she returned to Italy. © 2021 NautilusThink Inc,

Keyword: Apoptosis; Development of the Brain
Link ID: 28097 - Posted: 12.04.2021

By Emily Cataneo If you could upload your consciousness to the cloud and live forever as a mind in the metaverse, would you do it? Think carefully before answering. In “Feeling & Knowing: Making Minds Conscious,” neuroscientist Antonio Damasio argues that consciousness is far more than an algorithmic process. Uploading your consciousness to the cloud, he says, would be like experiencing a meal by reading a recipe rather than by eating. So then what is consciousness? That’s the question at the heart of this book. Damasio is a professor of neuroscience, philosophy, and psychology and the director of the Brain and Creativity Institute at the University of Southern California, Los Angeles, as well as the author of the 2018 book “The Strange Order of Things,” in which he extols the power of homeostasis, the force that keeps all living beings in equilibrium and therefore alive. Consciousness is such a slippery and ephemeral concept that it doesn’t even have its own word in many Romance languages, but nevertheless it’s a hot topic these days. “Feeling & Knowing” is the result of Damasio’s editor’s request to weigh in on the subject by writing a very short, very focused book. Over 200 pages, Damasio ponders profound questions: How did we get here? How did we develop minds with mental maps, a constant stream of images, and memories — mechanisms that exist symbiotically with the feelings and sensations in our bodies that we then, crucially, relate back to ourselves and associate with a sense of personhood?

Keyword: Consciousness
Link ID: 28096 - Posted: 12.04.2021

Daisy Yuhas Billions of people worldwide speak two or more languages. (Though the estimates vary, many sources assert that more than half of the planet is bilingual or multilingual.) One of the most common experiences for these individuals is a phenomenon that experts call “code switching,” or shifting from one language to another within a single conversation or even a sentence. This month Sarah Frances Phillips, a linguist and graduate student at New York University, and her adviser Liina Pylkkänen published findings from brain imaging that underscore the ease with which these switches happen and reveal how the neurological patterns that support this behavior are very similar in monolingual people. The new study reveals how code switching—which some multilingual speakers worry is “cheating,” in contrast to sticking to just one language—is normal and natural. Phillips spoke with Mind Matters editor Daisy Yuhas about these findings and why some scientists believe bilingual speakers may have certain cognitive advantages. Can you tell me a little bit about what drew you to this topic? I grew up in a bilingual household. My mother is from South Korea; my dad is African-American. So I grew up code switching a lot between Korean and English, as well as different varieties of English, such as African-American English and the more mainstream, standardized version. When you spend a lot of time code switching, and then you realize that this is something that is not well understood from a linguistic perspective, nor from a neurobiological perspective, you realize, “Oh, this is open territory.” © 2021 Scientific American

Keyword: Language
Link ID: 28095 - Posted: 12.01.2021

By Gretchen Reynolds Staying physically active as we age substantially drops our risk of developing dementia during our lifetimes, and it doesn’t require prolonged exercise. Walking or moving about, rather than sitting, may be all it takes to help bolster the brain, and a new study of octogenarians from Chicago may help to explain why. The study, which tracked how often older people moved or sat and then looked deep inside their brains after they passed away, found that certain vital immune cells worked differently in the brains of older people who were active compared to their more sedentary peers. Physical activity seemed to influence their brain’s health, their thinking abilities and whether they experienced the memory loss of Alzheimer’s disease. The findings add to growing evidence that when we move our bodies, we change our minds, no matter how advanced our age. Already, plenty of scientific evidence indicates that physical activity bulks up our brains. Older, sedentary people who begin walking for about an hour most days, for instance, typically add volume to their hippocampus, the brain’s memory center, reducing or reversing the shrinkage that otherwise commonly occurs there over the years. Active people who are middle-aged or older also tend to perform better on tests of memory and thinking skills than people of the same age who rarely exercise, and are nearly half as likely eventually to be diagnosed with Alzheimer’s disease. Almost as heartening, active people who do develop dementia usually show their first symptoms years later than inactive people do. But precisely how movement remodels our brains is still mostly mysterious, although scientists have hints from animal experiments. When adult lab mice and rats run on wheels, for example, they goose production of hormones and neurochemicals that prompt the creation of new neurons, as well as synapses, blood vessels and other tissues that connect and nurture those young brain cells. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 28094 - Posted: 12.01.2021

by Charles Q. Choi One injection of a potential new gene therapy for Angelman syndrome forestalls many of the neurodevelopmental condition’s key traits, according to early tests in mice. “While additional pharmacology and safety studies are needed, our viral vector can potentially provide transformative therapeutic relief with a single dose,” says lead investigator Benjamin Philpot, professor of neuroscience at the University of North Carolina at Chapel Hill. Angelman syndrome, which affects about one in 20,000 children, is associated with significant developmental delays and, often, autism. It arises from mutations or deletions in the maternal copy of the UBE3A gene, which encodes a protein that helps regulate the levels of other important proteins. There are no treatments specifically for Angelman syndrome, but several gene therapies are under development. One in clinical trials requires repeat injections in the spine and has shown serious side effects at high doses. These therapies all aim to restore UBE3A function in neurons. One challenge, though, is that neurons produce several variants, or ‘isoforms,’ of the UBE3A protein that vary slightly in length; in mice, for example, neurons make two isoforms in a ratio of about four short forms for every long one. In contrast to other gene therapies, the new one generates short and long forms of the UBE3A protein at nearly the same ratio as is seen in mouse neurons. Such proportions “may be important for therapeutic efficacy,” says Eric Levine, professor of neuroscience at the University of Connecticut in Farmington, who was not involved in this study. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28093 - Posted: 12.01.2021

By Ariana Remmel Scientists have finally sniffed out the molecules behind marijuana’s skunky aroma. The heady bouquet that wafts off of fresh weed is actually a cocktail of hundreds of fragrant compounds. The most prominent floral, citrusy and piney overtones come from a common class of molecules called terpenes, says analytical chemist Iain Oswald of Abstrax Tech, a private company in Tustin, Calif., that develops terpenes for cannabis products (SN: 4/30/18). But the source of that funky ganja note has been hard to pin down. Now, an analysis is the first to identify a group of sulfur compounds in cannabis that account for the skunklike scent, researchers report November 12 in ACS Omega. Oswald and colleagues had a hunch that the culprit may contain sulfur, a stinky element found in hops and skunk spray. So the team started by rating the skunk factor of flowers harvested from more than a dozen varieties of Cannabis sativa on a scale from zero to 10, with 10 being the most pungent. Next, the team created a “chemical fingerprint” of the airborne components that contributed to each cultivar’s unique scent using gas chromatography, mass spectroscopy and a sulfur chemiluminescence detector. As suspected, the researchers found small amounts of several fragrant sulfur compounds lurking in the olfactory profiles of the smelliest cultivars. The most dominant was a molecule called prenylthiol, or 3-methyl-2-butene-1-thiol, that gives “skunked beer” its notorious flavor (SN: 11/27/05). © Society for Science & the Public 2000–2021

Keyword: Chemical Senses (Smell & Taste); Drug Abuse
Link ID: 28092 - Posted: 12.01.2021

To eavesdrop on a brain, one of the best tools neuroscientists have is the fMRI scan, which helps map blood flow, and therefore the spikes in oxygen that occur whenever a particular brain region is being used. It reveals a noisy world. Blood oxygen levels vary from moment to moment, but those spikes never totally flatten out. “Your brain, even resting, is not going to be completely silent,” says Poortata Lalwani, a PhD student in cognitive neuroscience at the University of Michigan. She imagines the brain, even at its most tranquil, as kind of like a tennis player waiting to return a serve: “He’s not going to be standing still. He’s going to be pacing a little bit, getting ready to hit the backhand.” Many fMRI studies filter out that noise to find the particular spikes researchers want to scrutinize. But for Lalwani, that noise is the most telling signal of all. To her, it’s a signal of cognitive flexibility. Young, healthy brains tend to have signals with a lot of variability in blood oxygen levels from moment to moment. Older ones vary less, at least in certain regions of the brain. About a decade ago, scientists first showed the link between low neural signal variability and the kind of cognitive decline that accompanies healthy aging, rather than specific dementias. A brain’s noisiness is a solid proxy for details that are more abstract, Lalwani says: “How efficient information transfer is, how well-connected the neural networks are, in general how well-functioning the underlying neural network is.” But why that change happens with age has been a mystery. So has the question of whether it’s reversible. © 2021 Condé Nast.

Keyword: Attention; Alzheimers
Link ID: 28091 - Posted: 11.24.2021

By Kim Tingley When they first appeared in the United States in the mid-2000s, “electronic nicotine delivery systems” — e-cigarettes, vapes, e-liquids and other wares that contain the stimulant found in tobacco — were subject to little federal oversight. Their makers could incorporate countless other ingredients and flavorings. Like cigarettes before them, the devices proved extremely attractive to young people; in 2018, the surgeon general declared youth vaping an “epidemic” and noted that one in five high schoolers and one in 20 middle schoolers used e-cigarettes. Nicotine can harm the developing brain, and e-cigarettes contain potentially harmful toxins like heavy metals; the long-term effects of vaping — the heating of nicotine to create an inhaled aerosol — are uncertain. Despite these concerns, public-​health officials in the U.S. hope that, given a choice in the open market, people already addicted to nicotine will choose e-cigarettes over cigarettes — a deadly consumer product so successful at attracting and retaining users that it has killed as many as 24 million Americans over the past six decades. Because e-cigarettes generally contain fewer toxic chemicals than tobacco smoke, they are believed to be less damaging than cigarettes. If a sizable number of the one in seven adults in the U.S. who smoke switched to e-cigarettes, the theory goes, significantly fewer people might suffer from cancer and cardiovascular and respiratory diseases. In 2016, in an effort to mitigate the potential harms of e-cigarettes, the Food and Drug Administration began regulating them as “new tobacco products.” It became illegal to sell e-cigarettes to anyone under 18 (a cutoff that rose nationally to 21 in late 2019), and the agency was empowered to require warning labels. The F.D.A. also gained the authority to keep products out of the marketplace, unless it could be demonstrated that their public-health benefit outweighed their risks. (As a result of legislation passed in 2009, this condition applies to new tobacco products in general; cigarettes themselves, and other tobacco products on the market before Feb. 15, 2007, don’t have to meet the same standard.) As of last month, the agency had denied nearly a million applications. But a vaporizer and two liquids, in regular tobacco and menthol flavors, were authorized, after the F.D.A. declared that data submitted by their manufacturer showed that they were indeed less toxic than cigarettes and could, in the words of the agency’s news release, “benefit addicted adult smokers who switch to these products.” This would “outweigh the risk to youth” and lead to an overall “protection of the public health.” © 2021 The New York Times Company

Keyword: Drug Abuse
Link ID: 28090 - Posted: 11.24.2021

By Kelly Servick For patients whose depression resists treatment with drugs and electroconvulsive therapy, surgically implanted wires that stimulate the brain might bring relief. But in recent years, two randomized, controlled trials of this approach, known as deep brain stimulation (DBS), were halted after underwhelming results in interim analyses. “It was like the air was let out of the room,” Sameer Sheth, a neurosurgeon at Baylor College of Medicine, says of those results. “It was a big let-down.” Now, researchers are testing more sophisticated, personalized DBS techniques they hope will yield stronger results. The tests to date have involved just one or a few patients, far from proof of effectiveness. But researchers hope they’ll inform larger studies that finally cement the effectiveness of DBS in depression. “With all these irons in the fire … we will hopefully build up enough understanding and evidence,” says Sheth, an author of a case study published this week. DBS is already approved in the United States to treat epilepsy, obsessive compulsive disorder, and movement disorders such as Parkinson’s disease. Could it also shift patterns of abnormal activity in neural circuits that may drive depression symptoms? Early studies without control groups yielded promising results, but two randomized, controlled trials, sponsored by the medical device companies Medtronic and St. Jude Medical, Inc. (which was later acquired by Abbott Laboratories) did not show significant benefits after several months of DBS, teams reported in 2015 and 2017. Long-term follow-up of participants has revived some optimism. For example, many people in the 30-participant Medtronic trial improved over 1 year or more—beyond the timeline of the initial study, says Stanford University psychiatrist Mahendra Bhati, a co-investigator. Last month, he and colleagues published a follow-up study of eight trial patients, most of whom continue to use their implant about 10 years later. About one-half have had at least a 50% improvement over their pretreatment score on a depression scale. © 2021 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 28089 - Posted: 11.24.2021

By Gretchen Reynolds Does being active make us ravenous afterward and prone to eating more than we perhaps should? Or does it blunt our appetites and make it easier for us to skip that last, tempting slice of pie? A new study provides timely, if cautionary, clues. The study, which involved overweight, sedentary men and women and several types of moderate exercise, found that people who worked out did not overeat afterward at an enticing buffet lunch. However, they also did not skip dessert or skimp on portions. The findings offer a reminder during the holidays that while exercise has countless health benefits, helping us eat less or lose weight may not be among them. For most of us, exercise affects our weight and hunger in unexpected and sometimes contradictory ways. According to multiple scientific studies, few people who start to exercise drop as many pounds as the number of calories they burn working out would foretell. Some recent research suggests this occurs because our bodies stubbornly try to hang on to our fat stores, an evolutionary adaptation that protects us against (unlikely) future famines. So, if we burn calories during exercise, our bodies might nudge us to sit more afterward or reallocate energy from some bodily systems to others, reducing our overall daily energy expenditure. In this way, our bodies unconsciously compensate for many of the calories we burn exercising, reducing our chances of dropping pounds by working out. But that caloric compensation happens slowly, over the course of weeks or months, and involves energy expenditure. It has been less clear whether and how exercise influences our energy intake — that is, how many servings of food we consume — especially in the hours immediately after a workout. The evidence so far has been mixed. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 28088 - Posted: 11.24.2021

By Sabrina Imbler The male Bornean rock frog cannot scream over the sound of a waterfall. Instead, he threatens other frogs with his feet. The frog intimidates his male competitors with a can-can-like gesture: kicking his leg up into the air, fully extending his splayed foot, and dragging it down toward the ground. This foot-flagging display may not sound threatening to a human, but its effect has to do with a frog’s visual perception. To a frog, the world contains two kinds of objects: things that are worms, and things that are not worms. If a frog sees a skinny object moving parallel to its long axis — like how a worm travels along the ground — it sees dinner. But if a frog sees a similar shape moving perpendicular its long axis — very unlike a worm — it sees a threat to flee from. Scientists call this latter movement the anti-worm stimulus, and it strikes fear into the hearts of frogs. Frogs likely evolved this visual system to hunt worms and stay safe from larger predators. Now, researchers suggest some male frogs have evolved to take advantage of their froggy brethren’s fears by kicking and lowering their legs in a gesture that looks a lot like an anti-worm signal, as a way to frighten their competition. In a paper published Wednesday in Proceedings of the Royal Society B, researchers reveal that they could amplify the foot-flagging behavior of Bornean rock frogs by giving the frogs a dose of testosterone. The hormone acts on the muscles in the frog’s leg to exaggerate the gesture, meaning the more testosterone coursing through the frog, the bigger the foot-flagging display. This flamboyant foot display, intensified by the sex hormone, suggests the frogs evolved a way to exploit their competitors’ unusual visual system to appear more dangerous to other frogs. © 2021 The New York Times Company

Keyword: Aggression; Hormones & Behavior
Link ID: 28087 - Posted: 11.20.2021

ByEmily Underwood Scientists have argued for decades over whether humans have pheromones, chemical compounds that trigger aggression and mating in insects and other animals. Although the notion has great popular appeal—search Amazon for “pheromone” and you’ll get the idea—there’s scant evidence for this kind of signal in our species. A new study could change that. Researchers have identified an odorless compound emitted by people—and in particular babies—called hexadecanal, or HEX, that appears to foster aggressive behavior in women and blunt it in men. “We cannot say that this is a pheromone,” says study author Noam Sobel, a neuroscientist at the Weizmann Institute of Science. “But we can say that it’s a molecule expressed by the human body that influences human behavior, specifically aggressive behavior, in a predicted manner.” Humans emit HEX from their skin, saliva, and feces, and it’s among the most abundant molecules babies emit from their heads. When researchers isolated the odorless compound and piped it into mouse cages, it had a relaxing effect on the animals, says Sobel, who studies the role of scent in human interactions. To test how HEX affects people, Eva Mishor, who earned her Ph.D. in Sobel’s lab, created a series of computer games designed to evoke intense frustration—and a measurable response to it—in 126 human participants. Half of the volunteers wore a HEX-infused adhesive strip on their upper lips while they played, whereas the other half wore strips that smelled identical but were HEX-free. In one task, participants negotiated with an unseen partner to divvy up a sum of virtual money. The participants thought they were playing with another person, but they were actually playing against computers. If a player offered their “partner” anything less than 90% of the whole amount, the computer rejected their proposals with a bright red “NO!” preventing them from earning any money. © 2021 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 28086 - Posted: 11.20.2021

Yongsoo Kim The brain plays an essential role in how people navigate the world by generating both thought and behavior. Despite being one of the most vital organs of life, it takes up only 2% of human body volume. How can something so small perform such complex tasks? Luckily, modern tools like brain mapping have allowed neuroscientists like me to answer this exact question. By mapping out how all the cell types in the brain are organized and examining how they communicate with one another, neuroscientists can better understand how brains normally work, and what happens when certain cell parts go missing or malfunction. The task of understanding the inner workings of the brain has fascinated both philosophers and scientists for centuries. Aristotle proposed that the brain is where spirit resides. Leonardo da Vinci drew anatomical depictions of the brain with wax embedding. And Santiago Ramón y Cajal, with his 1906 Nobel Prize-winning work on the cellular structure of the nervous system, made one of the first breakthroughs that led to modern neuroscience as we know it. Using a new way to visualize individual cells called Golgi staining, a method pioneered by Nobel co-winner Camillo Golgi, and microscopic examination of brain tissue, Cajal established the seminal neuron doctrine. This principle states that neurons, among the main types of brain cells, communicate with one another via the gaps between them called synapses. These findings launched a race to understand the cellular composition of the brain and how brain cells are connected to one another. Conversation US, Inc.

Keyword: Brain imaging
Link ID: 28085 - Posted: 11.20.2021

by Niko McCarty Growing numbers of autistic children are diagnosed with the condition before age 3, in the United States, and those diagnoses tend to precede the start of any interventions or developmental services, according to a new study based on parent surveys. Children traversing autism’s ‘diagnostic odyssey’ a decade ago were typically diagnosed years later, and only after they had begun receiving services. The analysis included data from 2,303 autistic children aged 2 to 17 years from the National Survey of Children’s Health, which asks parents questions about the children in their household. The selected participants, split into three groups based on their age, either had a plan for early intervention or had received special services to meet developmental needs. The oldest children, aged 12 to 17 at the time of the survey, had been diagnosed at about age 5 and a half years, on average. Their first intervention or developmental service occurred at around age 5. By contrast, the youngest cohort, aged 2 to 5, had been diagnosed at about age 2 and a half years and started their first intervention or developmental services at roughly the same age. The results are based on parent responses to a question — “How old was your child when a doctor or other health care provider first said they had autism?” — so the findings likely skew toward younger ages than if the researchers had used clinical diagnoses. Also, the study omitted children who did not already have a diagnosis, which might have pushed the average age older. Still, the findings suggest that the time between getting a diagnosis and accessing services is shrinking. © 2021 Simons Foundation

Keyword: Autism
Link ID: 28084 - Posted: 11.20.2021

Riluzole, a drug approved to treat amyotrophic lateral sclerosis (ALS), a disease affecting nerve cells controlling movement, could slow the gradual loss of a particular brain cell that occurs in Niemann-Pick disease type C1 (NPC1), a rare genetic disorder affecting children and adolescents, suggests a study in mice by scientists at the National Institutes of Health. The study was conducted by Forbes D. Porter, M.D., Ph.D., of NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and colleagues in the National Human Genome Research Institute and National Institute of Arthritis and Musculoskeletal and Skin Disease. It appears in Molecular Genetics and Metabolism. The study was supported in part by a grant from the Ara Parseghian Medical Research Foundation. NPC1 results from an impaired ability to move cholesterol through cells, leading to difficulty controlling movements, liver and lung disease, impaired swallowing, intellectual decline and death. Much of the movement difficulties in NPC1 result from gradual loss of brain cells known as Purkinje neurons. The researchers found that mice with a form of NPC1 have a diminished ability to lower levels of glutamate — a brain chemical that stimulates neurons — after it has bound to a neuron’s surface. High levels of glutamate can be toxic to cells. The researchers believe the buildup of glutamate contributes to the brain cell loss seen in the disease. Riluzole blocks the release of glutamate and hence delays the progression of ALS in people.

Keyword: Movement Disorders
Link ID: 28083 - Posted: 11.20.2021

Andrew Gregory Health editor Drinking coffee or tea may be linked with a lower risk of stroke and dementia, according to the largest study of its kind. Strokes cause 10% of deaths globally, while dementia is one of the world’s biggest health challenges – 130 million are expected to be living with it by 2050. In the research, 365,000 people aged between 50 and 74 were followed for more than a decade. At the start the participants, who were involved in the UK Biobank study, self-reported how much coffee and tea they drank. Over the research period, 5,079 of them developed dementia and 10,053 went on to have at least one stroke. Researchers found that people who drank two to three cups of coffee or three to five cups of tea a day, or a combination of four to six cups of coffee and tea, had the lowest risk of stroke or dementia. Those who drank two to three cups of coffee and two to three cups of tea daily had a 32% lower risk of stroke. These people had a 28% lower risk of dementia compared with those who did not drink tea or coffee. The research, by Yuan Zhang and colleagues from Tianjin Medical University, China, suggests drinking coffee alone or in combination with tea is also linked with lower risk of post-stroke dementia. Writing in the journal Plos Medicine, the authors said: “Our findings suggested that moderate consumption of coffee and tea separately or in combination were associated with lower risk of stroke and dementia.” © 2021 Guardian News & Media Limited

Keyword: Stroke; Drug Abuse
Link ID: 28082 - Posted: 11.20.2021

Sophie Fessl Catching some z’s repairs a day’s damage to neurons’ DNA, at least in zebrafish. While the fish are awake, DNA damage accumulates, which, through a buildup of the DNA repair protein Parp1, triggers sleep, according to a study published today (November 18) in Molecular Cell. The study is “pivotal in providing evidence regarding sleep and its role in DNA damage and repair,” writes anesthesiologist Siu Wai Choi of the University of Hong Kong in an email to The Scientist. Choi led an earlier study that established a link between sleep deprivation and DNA damage in doctors but was not involved in the current research. Cells routinely face stress, such as exposure to radiation, that can leave their DNA damaged. Cells therefore have an arsenal of repair proteins to mend the DNA or, if it’s irreparable, trigger cell death. Neuroscientist Lior Appelbaum and his team at Bar-Ilan University in Israel had previously found that DNA damage increases during the day and decreases during the night, suggesting that sleep could help repair this damage. In the new study, they investigated whether DNA damage is the reason why zebrafish—and, by extension, perhaps other animals—sleep. When postdoc David Zada and other authors induced DNA damage in the neurons of zebrafish larvae by inducing neuronal activity or using UV radiation, the fish slept longer. “It makes the fish tired,” says Appelbaum. © 1986–2021 The Scientist.

Keyword: Sleep; Genes & Behavior
Link ID: 28081 - Posted: 11.20.2021

Anil Ananthaswamy How our brain, a three-pound mass of tissue encased within a bony skull, creates perceptions from sensations is a long-standing mystery. Abundant evidence and decades of sustained research suggest that the brain cannot simply be assembling sensory information, as though it were putting together a jigsaw puzzle, to perceive its surroundings. This is borne out by the fact that the brain can construct a scene based on the light entering our eyes, even when the incoming information is noisy and ambiguous. Consequently, many neuroscientists are pivoting to a view of the brain as a “prediction machine.” Through predictive processing, the brain uses its prior knowledge of the world to make inferences or generate hypotheses about the causes of incoming sensory information. Those hypotheses — and not the sensory inputs themselves — give rise to perceptions in our mind’s eye. The more ambiguous the input, the greater the reliance on prior knowledge. “The beauty of the predictive processing framework [is] that it has a really large — sometimes critics might say too large — capacity to explain a lot of different phenomena in many different systems,” said Floris de Lange, a neuroscientist at the Predictive Brain Lab of Radboud University in the Netherlands. However, the growing neuroscientific evidence for this idea has been mainly circumstantial and is open to alternative explanations. “If you look into cognitive neuroscience and neuro-imaging in humans, [there’s] a lot of evidence — but super-implicit, indirect evidence,” said Tim Kietzmann of Radboud University, whose research lies in the interdisciplinary area of machine learning and neuroscience. All Rights Reserved © 2021

Keyword: Attention; Vision
Link ID: 28080 - Posted: 11.17.2021