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Diana Kwon Susan was still a child when she first suspected something might be wrong with her mother. A cup or plate would often crash to the floor by accident when her mother was serving dinner or washing up dishes. “She was, she would have said, ‘clumsy’, but she wasn’t really clumsy,” says Susan. “Her hands had beautiful, glamorous movements, which I now recognize as early HD.” Huntington’s disease (HD) is an inherited condition that causes widespread deterioration in the brain and disrupts thinking, behaviour, emotion and movement. The disease usually begins in midlife, with subtle changes such as mood swings and difficulty in staying focused. As it progresses, people develop dementia and an inability to speak or move. Susan, who requested that her last name be withheld to protect her privacy, vividly remembers the day she learnt that her mother had the disease. It was the spring of 1982, and her mother had been admitted to a hospital because of her extreme exhaustion, frequent falls and irregular movements. There was no genetic test for the condition at the time, so she underwent a series of assessments. Her neurologist gathered the entire family into a room to break the news. “He told us that our mother had Huntington’s disease,” recalls Susan. “And that there’s no treatment and it can be wiped out in a generation if you just don’t breed.” Those blunt words had a profound impact on the lives of Susan and her siblings: her brother decided never to get married, and her sister chose to be sterilized. For Susan, however, those options were out of reach: she was pregnant when she received the news. © 2021 Springer Nature Limited

Keyword: Genes & Behavior; Movement Disorders
Link ID: 27762 - Posted: 04.08.2021

By Joshua Kendall When adults claim to have suddenly recalled painful events from their childhood, are those memories likely to be accurate? This question is the basis of the “memory wars” that have roiled psychology for decades. And the validity of buried trauma turns up as a point of contention in court cases and in television and movie story lines. Warnings about the reliability of a forgotten traumatic event that is later recalled—known formally as a delayed memory—have been endorsed by leading mental health organizations such as the American Psychiatric Association (APA). The skepticism is based on a body of research showing that memory is unreliable and that simple manipulations in the lab can make people believe they had an experience that never happened. Some prominent cases of recovered memory of child abuse have turned out to be false, elicited by overzealous therapists. But psychotherapists who specialize in treating adult survivors of childhood trauma argue that laboratory experiments do not rule out the possibility that some delayed memories recalled by adults are factual. Trauma therapists assert that abuse experienced early in life can overwhelm the central nervous system, causing children to split off a painful memory from conscious awareness. They maintain that this psychological defense mechanism—known as dissociative amnesia—turns up routinely in the patients they encounter. © 2021 Scientific American

Keyword: Stress; Learning & Memory
Link ID: 27761 - Posted: 04.08.2021

By Rachel Schraer People diagnosed with Covid-19 in the previous six months were more likely to develop depression, dementia, psychosis and stroke, researchers have found. A third of those with a previous Covid infection went on to develop or have a relapse of a psychological or neurological condition. But those admitted to hospital or in intensive care had an even higher risk. The study authors pointed to both the effects of stress, and the virus having a direct impact on the brain. UK scientists looked at the electronic medical records of more than half a million patients in the US, and their chances of developing one of 14 common psychological or neurological conditions, including: Anxiety and mood disorders were the most common diagnosis among those with Covid, and these were more likely to be down to the stress of the experience of being very ill or taken to hospital, the researchers explained. Conditions like stroke and dementia were more likely to be down to the biological impacts of the virus itself, or of the body's reaction to infection in general. Covid-19 was not associated with an increased risk of Parkinson's or Guillain-Barré syndrome (a risk from flu). Cause and effect The study, published in the Lancet Psychiatry journal, was observational. So the researchers couldn't say whether Covid had caused any of the diagnoses - and some people would have had a stroke or depression in the next six months regardless. But by comparing a group of people who had had Covid-19 with two groups - with flu and with other respiratory infections respectively - the researchers at the University of Oxford concluded Covid was associated with more subsequent brain conditions than other respiratory illnesses. © 2021 BBC.

Keyword: Depression; Alzheimers
Link ID: 27760 - Posted: 04.08.2021

By Jake Buehler Watch a group of lions yawn, and it may seem like nothing more than big, lazy cats acting sleepy, but new research suggests that these yawns may be subtly communicating some important social cues. Yawning is not only contagious among lions, but it appears to help the predators synchronize their movements, researchers report March 16 in Animal Behaviour. The discovery was partially made by chance, says Elisabetta Palagi, an ethologist at the University of Pisa in Italy. While studying play behavior in spotted hyenas in South Africa, she and colleagues often had the opportunity to watch lions (Panthera leo) at the same time. And she quickly noticed that lions yawn quite frequently, concentrating these yawns in short time periods. Yawning is ubiquitous among vertebrates, possibly boosting blood flow to the skull, cooling the brain and aiding alertness, especially when transitioning in and out of rest (SN: 9/8/15). Fish and reptiles will yawn, but more social vertebrates such as birds and mammals appear to have co-opted the behavior for purposes conducive to group living. In many species — like humans, monkeys, and even parakeets (SN: 6/1/15) — yawners can infect onlookers with their “yawn contagion,” leading onlookers to yawn shortly afterwards. Seeing the lions yawn reminded Palagi of her own work on contagious yawning in primates. Curious if the lions’ prodigious yawning was socially linked, Palagi and her team started recording videos of the big cats, analyzing when they were yawning and any behaviors around those times. © Society for Science & the Public 2000–2021

Keyword: Animal Communication; Stress
Link ID: 27759 - Posted: 04.08.2021

Jon Hamilton A study of mice that hear imaginary sounds could help explain human disorders like schizophrenia, which produce hallucinations. D-Keine/Getty Images A technique that induces imaginary sounds in both mice and people could help scientists understand the brain circuits involved in schizophrenia and other disorders that cause hallucinations. The technique appears to offer "a way to study psychotic disorders in animals," says Adam Kepecs, a professor of neuroscience and psychiatry at Washington University School of Medicine in St. Louis. It also shows how levels of the brain chemical dopamine determine the likelihood that a mouse or a person will perceive something that isn't really there, Kepecs and a team report in this week's issue of the journal Science. Until now, scientists have had no good way to study precisely how hallucinations occur in the brain. "This study is valuable because it will allow us to use mice and dig into the cellular, molecular, physiological details," says Eleanor Simpson, a researcher at the New York State Psychiatric Institute. That's important, Simpson says, because it could lead to better treatments for disorders like schizophrenia. "We have drugs that treat hallucinations but they're not very good," she says. "They don't work for everybody and they have a lot of terrible side effects which prevent people from using them." The study came about because "a mouse can't tell you when it's hallucinating," Kepecs © 2021 npr

Keyword: Schizophrenia; Hearing
Link ID: 27758 - Posted: 04.03.2021

By Benedict Carey When I joined the Science staff in 2004, reporters in the department had a saying, a reassuring mantra of sorts: “People will always come to the science section, if only to read about progress.” I think about that a lot as I say goodbye to my job, covering psychiatry, psychology, brain biology and big-data social science, as if they were all somehow related. The behavior beat, as it’s known, allowed tremendous freedom: I wrote about the mental upsides of binge drinking, playing the lotto and sports fandom. I covered basic lab research, the science of learning and memory, the experience of recurrent anguish, through the people who had to live with it. And much, much more. Like most science reporters, I had wanted to report on something big, to have a present-at-the-creation run that would shake up our understanding of mental health problems. At minimum, I expected research that would help people in distress improve their lives. But during my tenure, the science informing mental health care did not proceed smoothly along any trajectory. On the one hand, the field attracted enormous scientific talent, and there were significant discoveries, particularly in elucidating levels of consciousness in brain injury patients who appear unresponsive; and in formulating the first persuasive hypothesis of a cause for schizophrenia, based in brain biology. On the other hand, the science did little to improve the lives of the millions of people living with persistent mental distress. Almost every measure of our collective mental health — rates of suicide, anxiety, depression, addiction deaths, psychiatric prescription use — went the wrong direction, even as access to services expanded greatly. What happened? After 20 years covering the field, here and at The Los Angeles Times, I have a few theories, and some ideas on what might be required to turn things around. © 2021 The New York Times Company

Keyword: Depression; Stress
Link ID: 27757 - Posted: 04.03.2021

By Perri Klass, M.D. When parents bring their children in for medical care these days, there is no such thing as a casual, “Hey, how’s it going?” We doctors walk into every exam room prepared to hear a story of sadness and stress, or at the very least, of coping and keeping it together in this very hard year, full of isolation, loss, tragedy and hardship, with routines disrupted and comfort hard to come by. Parents have carried heavy burdens of stress and responsibility, worrying about themselves but also watching their children struggle, and there is worldwide concern about depression and suicidality among young people. But it isn’t only the adults and the young adults and teenagers who are suffering and sad; young children can also experience depression, but it can look very different, which makes it challenging for parents — or doctors — to recognize it and provide help. Rachel Busman, a clinical psychologist at the Child Mind Institute in New York City, said that it can be hard to think about depression in younger children because we picture childhood as a time of innocence and joy. But as many as 2 to 3 percent of children ages 6 to 12 can have serious depression, she said. And children with anxiety disorders, which are present in more than 7 percent of children aged 3 to 17, are also at risk for depression. Dr. Helen Egger, until recently the chair of child and adolescent psychiatry at N.Y.U. Langone Health, said that according to her epidemiologic research, between 1 and 2 percent of young children — as young as 3 — are depressed Depression was originally conceived of as an adult problem. Maria Kovacs, professor of psychiatry at the University of Pittsburgh School of Medicine, said that in the 1950s and ’60s, there were child psychiatrists who believed that children did not have sufficient ego development to feel depression, but that research that she and other colleagues did in the ’70s showed that “school age children can suffer from diagnosable depression.” © 2021 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 27756 - Posted: 04.03.2021

By Jake Buehler Fairy wrasses are swimming jewels, flitting and flouncing about coral reefs. The finger-length fishes’ brash, vibrant courtship displays are meant for mates and rivals, and a new study suggests that the slow waxing and waning of ice sheets and glaciers may be partly responsible for such a variety of performances. A new genetic analysis of more than three dozen fairy wrasse species details the roughly 12 million years of evolution that produced their vast assortment of shapes, colors and behaviors. And the timing of these transformations implies that the more than 60 species of fairy wrasses may owe their great diversity to cyclic sea level changes over the last few millions of years, scientists report February 23 in Systematic Biology. Within the dizzying assembly of colorful reef fishes, fairy wrasses (Cirrhilabrus) can’t help but stand out. They are the most species-rich genus in the second most species-rich fish family in the ocean, says Yi-Kai Tea, an ichthyologist at the University of Sydney. “That is quite a bit of biodiversity,” says Tea, who notes that new fairy wrasse species are identified every year. Despite this taxonomic footprint, Tea says, scientists knew “next to nothing” about the fairy wrasses’ evolutionary history or why there were so many species. © Society for Science & the Public 2000–2021.

Keyword: Sexual Behavior; Evolution
Link ID: 27755 - Posted: 04.03.2021

By Rachel Aviv Elizabeth Loftus was in Argentina, giving talks about the malleability of memory, in October, 2018, when she learned that Harvey Weinstein, who had recently been indicted for rape and sexual assault, wanted to speak with her. She couldn’t figure out how to receive international calls in her hotel room, so she asked if they could talk in three days, once she was home, in California. In response, she got a series of frantic e-mails saying that the conversation couldn’t wait. But, when Weinstein finally got through, she said, “basically he just wanted to ask, ‘How can something that seems so consensual be turned into something so wrong?’ ” Loftus, a professor at the University of California, Irvine, is the most influential female psychologist of the twentieth century, according to a list ­compiled by the Review of General Psychology. Her work helped usher in a paradigm shift, rendering obsolete the archival model of memory—the idea, dominant for much of the twentieth century, that our memories exist in some sort of mental library, as literal representations of past events. According to Loftus, who has published twenty-four books and more than six hundred papers, memories are reconstructed, not replayed. “Our representation of the past takes on a living, shifting reality,” she has written. “It is not fixed and immutable, not a place way back there that is preserved in stone, but a living thing that changes shape, expands, shrinks, and expands again, an amoeba-­like creature.” George A. Miller, one of the founders of cognitive psychology, once said in a speech to the American Psychological Association that the way to advance the field was “to give psychology away.” Loftus, who is seventy-six, adopts a similar view, seizing any opportunity to elaborate on what she calls the “flimsy curtain that separates our imagination and our memory.” In the past forty-five years, she has testified or consulted in more than three hundred cases, on behalf of people wrongly accused of robbery and murder, as well as for high-profile defendants like Bill Cosby, Jerry Sandusky, and the Duke lacrosse players accused of rape, in 2006. “If the MeToo movement had an office, Beth’s picture would be on the ten-most-wanted list,” her brother Robert told me. © 2021 Condé Nast.

Keyword: Learning & Memory
Link ID: 27754 - Posted: 03.31.2021

By Lisa Sanders, M.D. The dental hygienist greeted her longtime patient enthusiastically. Unexpectedly, the 68-year-old woman burst into tears. “I feel so bad,” she said, her voice cracking with emotion. “I’m worried I might be dying.” She was always tired, as if all her energy had been sucked out. And she felt a strange dread that something awful was happening to her. And if that weren’t enough, for the past couple of weeks she had lost much of her hearing in her right ear. She was sure she had a brain tumor — though none of her doctors thought so. After offering sympathy, the dental assistant realized she had something more to offer: “We have a dental CT scanner. Should we get a CT of your head?” The patient was amazed. Yes — she would very much like a CT scan of her head. It would cost her $150, the technician told her. At that point, it seemed like a bargain. And, just like that, it was done. And there was a mass. It wasn’t on the right side, where she thought her trouble lay. It was on the left. And it wasn’t in her ear, but in the sinus behind her cheek. That was confusing. She thanked the tech for the scan. She had an ENT and would send the images to him to see what he thought. That right ear had been giving the patient trouble for more than 20 years, she reminded her ear, nose and throat doctor in Prescott, Ariz., when she spoke with him. In her 40s she developed terrible vertigo. She was living in Atlanta then and saw an ENT there who told her she probably had Ménière’s disease, a disorder induced by increased pressure in the inner ear. The cause is unknown, though in some cases it appears to run in families. And it’s characterized by intermittent episodes of vertigo usually accompanied by a sensation of fullness in the ear, as well as tinnitus and hearing loss. These symptoms can be present from the start, but often develop over time. There’s no definitive test for the disease, though evidence of the increased pressure is sometimes visible on an M.R.I. © 2021 The New York Times Company

Keyword: Hearing
Link ID: 27753 - Posted: 03.31.2021

By Kathryn Schulz One of the most amazing things I have ever witnessed involved an otherwise unprepossessing house cat named Billy. This was some years ago, shortly after I had moved into a little rental house in the Hudson Valley. Billy, a big, bad-tempered old tomcat, belonged to the previous tenant, a guy by the name of Phil. Phil adored that cat, and the cat—improbably, given his otherwise unenthusiastic feelings about humanity—returned the favor. On the day Phil vacated the house, he wrestled an irate Billy into a cat carrier, loaded him into a moving van, and headed toward his new apartment, in Brooklyn. Thirty minutes down I-84, in the middle of a drenching rainstorm, the cat somehow clawed his way out of the carrier. Phil pulled over to the shoulder but found that, from the driver’s seat, he could neither coax nor drag the cat back into captivity. Moving carefully, he got out of the van, walked around to the other side, and opened the door a gingerly two inches—whereupon Billy shot out, streaked unscathed across two lanes of seventy-mile-per-hour traffic, and disappeared into the wide, overgrown median. After nearly an hour in the pouring rain trying to make his own way to the other side, Phil gave up and, heartbroken, continued onward to his newly diminished home. Some weeks later, at a little before seven in the morning, I woke up to a banging at my door. Braced for an emergency, I rushed downstairs. The house had double-glass doors flanked by picture windows, which together gave out onto almost the entire yard, but I could see no one. I was standing there, sleep-addled and confused, when up onto his hind legs and into my line of vision popped an extremely scrawny and filthy gray cat. I gaped. Then I opened the door and asked the cat, idiotically, “Are you Billy?” He paced, distraught, and meowed at the door. I retreated inside and returned with a bowl each of food and water, but he ignored them and banged again at the door. Flummoxed, I took a picture and texted it to my landlord with much the same question I had asked the cat: “Is this Billy?” © 2021 Condé Nast.

Keyword: Animal Migration
Link ID: 27752 - Posted: 03.31.2021

By Gretchen Reynolds Brisk walking improves brain health and thinking in aging people with memory impairments, according to a new, yearlong study of mild cognitive impairment and exercise. In the study, middle-aged and older people with early signs of memory loss raised their cognitive scores after they started walking frequently. Regular exercise also amplified the healthy flow of blood to their brains. The changes in their brains and minds were subtle but consequential, the study concludes, and could have implications not just for those with serious memory problems, but for any of us whose memories are starting to fade with age. Most of us, as we get older, will find that our ability to remember and think dulls a bit. This is considered normal, if annoying. But if the memory loss intensifies, it may become mild cognitive impairment, a medical condition in which the loss of thinking skills grows obvious enough that it becomes worrisome to you and others around you. Mild cognitive impairment is not dementia, but people with the condition are at heightened risk of developing Alzheimer’s disease later. Scientists have not yet pinpointed the underlying causes of mild cognitive impairment, but there is some evidence that changes in blood flow to the brain can contribute. Blood carries oxygen and nutrients to brain cells and if that stream sputters, so can the vitality of neurons. Unfortunately, many people experience declines in the flow of blood to their brains with age, when their arteries stiffen and hearts weaken. © 2021 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27751 - Posted: 03.31.2021

Jennifer Hellmann Parents who are exposed to predators pass on information about risky environments to their offspring through changes in gene expression – but how that information affects offspring differs depending on the sex of the parent. My colleagues and I showed this using sticklebacks – a small species of freshwater fish whose brightly colored males care for developing eggs – in a series of papers recently published in the Journal of Animal Ecology. First, we exposed mothers and fathers to predators. Then we looked at their offspring and measured behavior as well as how genes were expressed in their brains. We found that the sex of the parent exposed to predators matters, but surprisingly, the sex of the offspring also changed how the information influenced behavior. Predator‐exposed fathers produced bolder sons that took more risks, but the father’s experiences had no effect on the boldness of daughters. Predator‐exposed mothers, on the other hand, produced more anxious daughters and also more anxious sons. These sons and daughters had different patterns of gene expression, matching our behavioral results. We also studied whether these changes persisted into a second generation. In grandkids, we again found complicated patterns of sex-specific inheritance. So how does this work? It’s not that experiences have changed what genes the parents pass on. Rather, what changes is how those genes are expressed in the offspring. This variability in gene expression is called epigenetics. Stickleback eggs showing embryos growing inside. Through epigenetics, a parent can pass down information to the next generation of sticklebacks like the ones growing in these eggs. Jennifer Hellman, CC BY-ND © 2010–2021, The Conversation US, Inc.

Keyword: Epigenetics; Stress
Link ID: 27750 - Posted: 03.31.2021

By Laura Sanders Octopuses cycle through two stages of slumber, a new study reports. First comes quiet sleep, and then a shift to a twitchy, active sleep in which vibrant colors flash across the animals’ skin. These details, gleaned from four snoozing cephalopods in a lab in a Brazil, may provide clues to a big scientific mystery: Why do animals sleep? Sleep is so important that every animal seems to have a version of it, says Philippe Mourrain, a neurobiologist at Stanford University who recently described the sleep stages of fish (SN: 7/10/19). Scientists have also catalogued sleep in reptiles, birds, amphibians, bees, mammals and jellyfish, to name a few. “So far, we have not found a single species that does not sleep,” says Mourrain, who was not involved in the new study. Cephalopod neuroscientist and diver Sylvia Medeiros caught four wild octopuses, Octopus insularis, and brought them temporarily into a lab at the Brain Institute of the Federal University of Rio Grande do Norte in Natal, Brazil. After tucking the animals away in a quiet area, she began to carefully record their behavior during the day, when octopuses are more likely to rest. Two distinct states emerged, she and her colleagues report March 25 in iScience. In the first, called quiet sleep, the octopuses are pale and motionless with the pupils of their eyes narrowed to slits. Active sleep comes next. Eyes dart around, suckers contract, muscles twitch, skin textures change and, most dramatically, bright colors race across octopuses’ bodies. This wild sleep is rhythmic, happening every half an hour or so, and brief; it’s over after about 40 seconds. Active sleep is also rare; the octopuses spent less than 1 percent of their days in active sleep, the researchers found. © Society for Science & the Public 2000–2021.

Keyword: Sleep; Evolution
Link ID: 27749 - Posted: 03.27.2021

By Veronique Greenwood There’s nothing quite like the peculiar, bone-jarring reaction of a damaged tooth exposed to something cold: a bite of ice cream, or a cold drink, and suddenly, that sharp, searing feeling, like a needle piercing a nerve. Researchers have known for years that this phenomenon results from damage to the tooth’s protective outer layer. But just how the message goes from the outside of your tooth to the nerves within it has been difficult to uncover. On Friday, biologists reported in the journal Science Advances that they have identified an unexpected player in this painful sensation: a protein embedded in the surface of cells inside the teeth. The discovery provides a glimpse of the connection between the outer world and the interior of a tooth, and could one day help guide the development of treatments for tooth pain. More than a decade ago, Dr. Katharina Zimmerman, now a professor at Friedrich-Alexander University in Germany, discovered that cells producing a protein called TRPC5 were sensitive to cold. When things got chilly, TRPC5 popped open to form a channel, allowing ions to flow across the cell’s membrane. Ion channels like TRPC5 are sprinkled throughout our bodies, Dr. Zimmerman said, and they are behind some surprisingly familiar sensations. For instance, if your eyes start to feel cold and dry in chilly air, it’s a result of an ion channel being activated in the cornea. She wondered which other parts of the body might make use of a cold receptor such as TRPC5. And it occurred to her that “the most sensitive tissue in the human body can be teeth” when it comes to cold sensations. © 2021 The New York Times Company

Keyword: Pain & Touch
Link ID: 27748 - Posted: 03.27.2021

By Erin Garcia de Jesús One defective gene might turn some bunnies’ hops into handstands, a new study suggests. To move quickly, a breed of domesticated rabbit called sauteur d’Alfort sends its back legs sky high and walks on its front paws. That strange gait may be the result of a gene tied to limb movement, researchers report March 25 in PLOS Genetics. Sauteur d’Alfort rabbits aren’t the only animal to adopt an odd scamper if there’s a mutation to this gene, known as RORB. Mice with a mutation to the gene also do handstands if they start to run, says Stephanie Koch, a neuroscientist at University College London who was not involved with the rabbit work. And even while walking, the mice hike their back legs up to waddle forward, almost like a duck. “I spent four years looking at these mice doing little handstands, and now I get to see a rabbit do the same handstand,” says Koch, who led a 2017 study published in Neuron that explored the mechanism behind the “duck gait” in mice. “It’s amazing.” Understanding why the rabbits move in such a strange way could help researchers learn more about how the spinal cord works. The study is “contributing to our basic knowledge about a very important function in humans and all animals — how we are able to move,” says Leif Andersson, a molecular geneticist at Uppsala University in Sweden. © Society for Science & the Public 2000–2021.

Keyword: Genes & Behavior; Movement Disorders
Link ID: 27747 - Posted: 03.27.2021

by Angie Voyles Askham Mice that lack CNTNAP2, a gene linked to autism, have an atypical collection of microbes in their intestines, according to a new study. Treating the mice with a strain of gut bacteria commonly found in wildtype mice, people and other mammals improves their social behavior. The CNTNAP2 mice are hyperactive, and those raised in isolation prefer to spend time alone or with a familiar cagemate rather than with a stranger mouse. But when they grow up alongside wildtype littermates, their social deficits — but not their hyperactivity — disappear, the study shows. Because mice that live together eat one another’s feces, which can alter the microbial content of their guts, the researchers wondered if a change in the microbiome might be driving the change in the isolated animals’ social behaviors. “It was sort of a serendipitous discovery,” says lead investigator Mauro Costa-Mattioli, professor of neuroscience at Baylor College of Medicine in Houston, Texas. The findings highlight how some autism traits associated with genetic mutations may be shaped, and potentially eased, via changes to the gut microbiome. Figuring out which behaviors can be attributed to the environment is particularly helpful for thinking about treatments because the environment can be changed, whereas “genetics is still hard to correct,” says Sarkis Mazmanian, professor of microbiology at the California Institute of Technology in Pasadena, who was not involved in the work. © 2021 Simons Foundation

Keyword: Autism
Link ID: 27746 - Posted: 03.27.2021

By Christina Caron When Laura Drager contracted Covid-19 in July, it was as though someone had suddenly muted her olfactory system. One morning she was sipping her favorite Gatorade (the yellow one), and two hours later the drink was completely flavorless. She immediately lit a candle and blew it out, but she couldn’t smell the smoke. Her sense of smell had disappeared. Now, she said, “everything either tastes like bleach or tastes like nothing.” Over the past few months she has lost 19 pounds. “I don’t have that ‘I’m hungry’ feeling,” said Ms. Drager, 41, who lives in Sevierville, Tenn., about 45 minutes from Knoxville. “I think you forget how much smell and taste is a part of your life until it goes away.” As the coronavirus continues to spread, there are increasing numbers of people who have either lost their senses of smell after contracting Covid or are struggling with parosmia, a disturbing disorder that causes previously normal odors to develop a new, often unpleasant aroma. One meta-analysis published in September found that as many as 77 percent of those who had Covid were estimated to have some form of smell loss as a result of their infections. The recommended treatment for these conditions is smell training. But how exactly do you do it, and why should you bother? © 2021 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27745 - Posted: 03.27.2021

Researchers at the National Institutes of Health (NIH) have discovered specific regions within the DNA of neurons that accumulate a certain type of damage (called single-strand breaks or SSBs). This accumulation of SSBs appears to be unique to neurons, and it challenges what is generally understood about the cause of DNA damage and its potential implications in neurodegenerative diseases. Because neurons require considerable amounts of oxygen to function properly, they are exposed to high levels of free radicals—toxic compounds that can damage DNA within cells. Normally, this damage occurs randomly. However, in this study, damage within neurons was often found within specific regions of DNA called “enhancers” that control the activity of nearby genes. Fully mature cells like neurons do not need all of their genes to be active at any one time. One way that cells can control gene activity involves the presence or absence of a chemical tag called a methyl group on a specific building block of DNA. Closer inspection of the neurons revealed that a significant number of SSBs occurred when methyl groups were removed, which typically makes that gene available to be activated. An explanation proposed by the researchers is that the removal of the methyl group from DNA itself creates an SSB, and neurons have multiple repair mechanisms at the ready to repair that damage as soon as it occurs. This challenges the common wisdom that DNA damage is inherently a process to be prevented. Instead, at least in neurons, it is part of the normal process of switching genes on and off. Furthermore, it implies that defects in the repair process, not the DNA damage itself, can potentially lead to developmental or neurodegenerative diseases.

Keyword: Epigenetics; Parkinsons
Link ID: 27744 - Posted: 03.27.2021

By Karen J. Bannan Hayley Gudgin of Sammamish, Wash., got her first migraine in 1991 when she was a 19-year-old nursing student. “I was convinced I was having a brain hemorrhage,” she says. “There was no way anything could be that painful and not be really serious.” She retreated to her bed and woke up feeling better the next day. But it wasn’t long until another migraine hit. And another. Taking a pill that combines caffeine with the pain relievers acetaminophen and codeine made life manageable until she got pregnant and had to stop taking her medication. After her son was born, the migraines came back. She started taking the drugs again, but they didn’t work and actually made her attacks worse. By the time Gudgin gave birth to her second son in 1997, she was having about 15 attacks a month. Her symptoms worsened over time and included severe pain, nausea, sensitivity to light, swollen hands, difficulty speaking, vomiting and diarrhea so intense she often wound up dehydrated in the emergency room. “It hit me [that] I had to do something when I was vomiting in the toilet, and my 3-year-old came and pulled my hair back,” she says. “It was no way to live — and not just because of the pain. You go to sleep every night not knowing how you’re going to wake up. You make plans knowing you might have to cancel them.” A headache specialist prescribed several preventive medicines, but each caused side effects for Gudgin, including weight gain and kidney stones. Then, in 2018, Gudgin read about a new type of treatment for frequent migraine sufferers. Her neurologist agreed it was worth a try. After much wrangling with her insurance company — the drug is costly, and she had to prove that two other drugs had failed to help her — she got approval to take it. © Society for Science & the Public 2000–2021.

Keyword: Pain & Touch
Link ID: 27743 - Posted: 03.23.2021