Heidi Ledford Under the right circumstances, even moderately hungry mice prefer to socialize with the opposite sex than to eat, researchers have found1. In research published on 23 February in Cell Metabolism, scientists treated male mice with a technique that mimics the effects of leptin, a hormone that acts on the brain to suppress appetite. Treated mice were more likely to approach female mice than their food bowls — even if the test rodents had been deprived of food for almost an entire day. The findings reveal a surprising role for leptin in social behaviour. They are also a step towards understanding how animals prioritize different behavioural options in response to ongoing needs — an enduring question in neuroscience, says Gina Leinninger, who studies the neural regulation of feeding at Michigan State University in East Lansing. The paper “addresses a huge gap in the field”, she says. “When you no longer need to eat urgently, it should free you up to do other things.” The new work, Leinninger says, illuminates how the brain juggles these various demands. Food versus friends Neuroscientists Anne Petzold and Tatiana Korotkova at the University of Cologne in Germany, and their colleagues, sought to understand how such decision-making is affected by leptin, which activates a subset of cells in the brain and promotes a feeling of fullness. The researchers injected male mice with leptin and saw that it suppressed feeding, as expected — but also promoted interactions with female mice. The team examined neurons in the brain’s ‘hunger center’, the lateral hypothalamus, that are activated by leptin. The authors’ experiments showed that neurons that can sense leptin were activated when mice interacted with members of the opposite sex. Artificially activating those neurons using a technique called optogenetics raised the likelihood that a mouse would approach a member of the opposite sex. Both results suggest that leptin plays a part in promoting social behaviour. © 2023 Springer Nature Limited

Keyword: Obesity; Sexual Behavior
Link ID: 28682 - Posted: 02.25.2023

By Virat Markandeya It’s evening at the northern tip of the Red Sea, in the Gulf of Aqaba, and Tom Shlesinger readies to take a dive. During the day, the seafloor is full of life and color; at night it looks much more alien. Shlesinger is waiting for a phenomenon that occurs once a year for a plethora of coral species, often several nights after the full moon. Guided by a flashlight, he spots it: coral releasing a colorful bundle of eggs and sperm, tightly packed together. “You’re looking at it and it starts to flow to the surface,” Shlesinger says. “Then you raise your head, and you turn around, and you realize: All the colonies from the same species are doing it just now.” Some coral species release bundles of a pinkish- purplish color, others release ones that are yellow, green, white or various other hues. “It’s quite a nice, aesthetic sensation,” says Shlesinger, a marine ecologist at Tel Aviv University and the Interuniversity Institute for Marine Sciences in Eilat, Israel, who has witnessed the show during many years of diving. Corals usually spawn in the evening and night within a tight time window of 10 minutes to half an hour. “The timing is so precise, you can set your clock by the time it happens,” Shlesinger says. Moon-controlled rhythms in marine critters have been observed for centuries. There is calculated guesswork, for example, that in 1492 Christopher Columbus encountered a kind of glowing marine worm engaged in a lunar-timed mating dance, like the “flame of a small candle alternately raised and lowered.” Diverse animals such as sea mussels, corals, polychaete worms and certain fishes are thought to synchronize their reproductive behavior by the moon. The crucial reason is that such animals — for example, over a hundred coral species at the Great Barrier Reef — release their eggs before fertilization takes place, and synchronization maximizes the probability of an encounter between eggs and sperm. © 2023 Annual Reviews

Keyword: Biological Rhythms; Sexual Behavior
Link ID: 28681 - Posted: 02.25.2023

Diana Kwon Hundreds of scientists around the world are looking for ways to treat heart attacks. But few started where Hedva Haykin has: in the brain. Haykin, a doctoral student at the Technion — Israel Institute of Technology in Haifa, wants to know whether stimulating a region of the brain involved in positive emotion and motivation can influence how the heart heals. Late last year, in a small, windowless microscope room, she pulled out slides from a thin black box, one by one. On them were slices of hearts, no bigger than pumpkin seeds, from mice that had experienced heart attacks. Under a microscope, some of the samples were clearly marred by scars left in the aftermath of the infarction. Others showed mere speckles of damage visible among streaks of healthy, red-stained cells. The difference in the hearts’ appearance originated in the brain, Haykin explains. The healthier-looking samples came from mice that had received stimulation of a brain area involved in positive emotion and motivation. Those marked with scars were from unstimulated mice. “In the beginning we were sure that it was too good to be true,” Haykin says. It was only after repeating the experiment several times, she adds, that she was able to accept that the effect she was seeing was real. Haykin, alongside her supervisors at the Technion — Asya Rolls, a neuroimmunologist, and Lior Gepstein, a cardiologist — are trying to work out exactly how this happens. On the basis of their experiments so far, which have not yet been published, activation of this brain reward centre — called the ventral tegmental area (VTA) — seems to trigger immune changes that contribute to the reduction of scar tissue. This study has its roots in decades of research pointing to the contribution of a person’s psychological state to their heart health1. In a well-known condition known as ‘broken-heart syndrome’, an extremely stressful event can generate the symptoms of a heart attack — and can, in rare cases, be fatal. Conversely, studies have suggested that a positive mindset can lead to better outcomes in those with cardiovascular disease. But the mechanisms behind these links remain elusive.

Keyword: Neuroimmunology
Link ID: 28680 - Posted: 02.25.2023

Kevin Rawlinson It is no mystery that a good night’s sleep and a lie-in can improve your day. But researchers are suggesting that, far from just being enjoyable, quality sleep may even add years to people’s lives. Men who regularly sleep well could live almost five years longer than those who do not, while women could benefit by two years, research suggests. And they could also enjoy better health during their lives. Researchers found that young people who had better sleep habits were less likely to die early. But the researchers said their findings indicated quantity of sleep was not in itself enough to achieve the possible health benefits – quality of sleep is also important. Good sleep was based on five different factors: ideal sleep duration of seven to eight hours a night; difficulty falling asleep no more than two times a week; trouble staying asleep no more than two times a week; not using any sleep medication; and feeling well rested after waking up at least five days a week. The findings suggested that about 8% of deaths from any cause could be attributed to poor sleep patterns. Dr Frank Qian, an internal medicine resident physician at Beth Israel Deaconess Medical Center in Boston, America, said: “We saw a clear dose-response relationship, so the more beneficial factors someone has in terms of having higher quality of sleep, they also have a stepwise lowering of all cause and cardiovascular mortality.” © 2023 Guardian News & Media Limited

Keyword: Sleep
Link ID: 28679 - Posted: 02.25.2023

By Darren Incorvaia Sitting in an exam room, surrounded by doctors and scientists, Heather Rendulic opened her left hand for the first time since suffering a series of strokes nine years earlier when she was in her early 20s. “It was an amazing feeling for me to be able to do that again,” Rendulic says. “It’s not something I ever thought was possible.” But immediately after a surgically implanted device sent electrical pulses into her spinal cord, Rendulic could not only open her hand but also showed other marked improvements in arm mobility, researchers report February 20 in Nature Medicine. “We all started crying,” Marco Capogrosso, a neuroscientist at the University of Pittsburgh, said in a February 15 news conference. “We didn’t really expect this could work as fast as that.” The approach is similar to that recently used for patients paralyzed by spinal cord injuries (SN: 08/03/22). It represents a promising new technique for restoring voluntary movement to those left with upper-body paralysis following strokes, the team says. A stroke occurs when blood supply to parts of the brain is cut off, often causing short-term or long-term issues with movement, speech and vision. Stroke is a leading, and often underappreciated, cause of paralysis; in the United States alone, 5 million people are living with some form of motor deficit due to stroke. While physical therapy can provide some improvements, no treatment exists to help these patients regain full control of their limbs — and their lives. Strokes cause paralysis because the connection between the brain and the spinal cord is damaged; the brain tries to tell the spinal cord to move certain muscles, but the message is muddled. © Society for Science & the Public 2000–2023.

Keyword: Stroke; Robotics
Link ID: 28678 - Posted: 02.22.2023

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

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

By Dani Blum There are a few tried and true pieces of advice that sleep doctors always give for battling insomnia: Watch those alcoholic drinks at dinner, cut the afternoon coffee, stop scrolling before bed. And please, they beg: Keep your sleep schedule consistent. Flip-flopping between wake-up times — jolting awake at 7:30 on a Friday morning and then dozing until the afternoon on Saturday — wreaks havoc on our internal body clocks. Sleep experts refer to this as “social jet lag,” said Dr. Sabra Abbott, a sleep medicine specialist at the Northwestern Feinberg School of Medicine. Similar to changing time zones, heading to bed at vastly different times from night to night may throw off your circadian rhythm. And still, as anyone who’s worked a night shift, taken care of a toddler or fumbled back home after a party might tell you: Going to bed and waking up at the same times is easier said than done. “It’s a luxury, right?” said Kelsie Full, a behavioral epidemiologist and an assistant professor at Vanderbilt University Medical Center. Dr. Full is the lead author of a new study that tied irregular sleep to an early marker of cardiovascular disease. Researchers examined a week’s worth of sleep data from 2,000 adults over 45 and found that those who slept varying amounts each night and went to bed at different times were more likely to have hardened arteries than those with more regular sleep patterns. People whose overall sleep amounts varied by two or more hours from night to night throughout the week — getting five hours of sleep on Tuesday, say, and then eight hours on Wednesday — were particularly likely to have high levels of calcified fatty plaque built up in their arteries, compared with those who slept the same number of hours each night. The study could not confirm that inconsistent sleep patterns definitively caused the heart issues, Dr. Full said. And the findings don’t necessarily mean that the occasional late night or very early morning should be off the table. © 2023 The New York Times Company

Keyword: Sleep
Link ID: 28676 - Posted: 02.22.2023

By Dani Blum The family of Bruce Willis announced that the actor has frontotemporal dementia, known as FTD, a form of dementia that occurs most commonly when nerve cells in the frontal and temporal lobes of the brain decrease in number. Mr. Willis, 67, was previously diagnosed with aphasia, which prompted him to retire from acting. “FTD is a cruel disease that many of us have never heard of and can strike anyone,” the family wrote in a statement. There are two main variants of FTD: primary progressive aphasia, which hampers a patient’s ability to communicate, and behavioral variant frontotemporal dementia, which manifests as personality and behavioral changes. “It hits the parts of the brain that make us the most human,” said Dr. Bruce Miller, a professor of neurology at the University of California, San Francisco. FTD is the most common cause of dementia for people under the age of 60, said Susan Dickinson, the chief executive of the Association for Frontotemporal Degeneration. There are roughly 50,000 people in the United States with a diagnosis of FTD, she added, although many experts consider that number to be a vast undercount, because of how challenging it can be to diagnose. There is no blood test or single biomarker to diagnose the condition — doctors instead identify it based on symptoms and neuroimaging. On average, it takes patients more than three years to get an accurate diagnosis, Ms. Dickinson said. People with primary progressive aphasia may struggle to speak in full sentences or have difficulty comprehending conversations. They may have a hard time writing or reading. Those with the behavioral variant of FTD may act out of character, said Dr. Ian Grant, an assistant professor of neurology at the Northwestern University Feinberg School of Medicine. Families will say that patients “seem like they’ve lost a little bit of their filter,” he said. Someone who is typically quiet and reserved may start spewing profanities, for example, or loudly comment on a stranger’s appearance. The person may act apathetic, Dr. Miller said, losing motivation. Some may also display a lack of empathy for those around them. © 2023 The New York Times Company

Keyword: Alzheimers; Language
Link ID: 28675 - Posted: 02.18.2023

Max Kozlov A group of brain cells in mice becomes active both when the animals fight and when they watch other mice fight, a study1 shows. The work hints that such ‘mirror neurons’, which fire when an animal either observes or takes part in a particular activity, could shape complex social behaviours, such as aggression. The mirror neurons described in the study are the first to be found in the hypothalamus, an evolutionarily ancient brain region — suggesting that mirror neurons’ original purpose might have been to enhance defence and, ultimately, reproductive success, the authors speculate. The study was published in Cell on 15 February. “We’ve now shown that mirror neurons functionally participate in the behaviours they’re mirroring,” says Nirao Shah, a neuroscientist at Stanford University in California who co-authored the study. “That changes what we think about mirror neurons.” First identified in monkeys in the 1990s, mirror neurons generally fire when an animal takes a certain action, but they also fire when it sees another animal perform the same action. Previous work has linked mirror neurons’ activity to simple behaviours, such as reaching for an object, but not to complex social behaviours, such as fighting. But exactly how mirror-neuron activity contributes to cognitive functions has been controversial, says Pier Francesco Ferrari, a neuroethologist at the Institute of Cognitive Science Marc Jeannerod in Lyon, France. Some researchers have argued that the fact that mirror neurons fire both when an animal observes a behaviour and when it performs that behaviour itself shows that these neurons are involved in a higher-order awareness of others’ actions — and perhaps even contribute to empathy. But others say that there is little evidence to support this theory. © 2023 Springer Nature Limited

Keyword: Aggression; Attention
Link ID: 28674 - Posted: 02.18.2023

By McKenzie Prillaman Psychedelics go beneath the cell surface to unleash their potentially therapeutic effects. These drugs are showing promise in clinical trials as treatments for mental health disorders (SN: 12/3/21). Now, scientists might know why. These substances can get inside nerve cells in the cortex — the brain region important for consciousness — and tell the neurons to grow, researchers report in the Feb. 17 Science. Several mental health conditions, including depression and post-traumatic stress disorder, are tied to chronic stress, which degrades neurons in the cortex over time. Scientists have long thought that repairing the cells could provide therapeutic benefits, like lowered anxiety and improved mood. Psychedelics — including psilocin, which comes from magic mushrooms, and LSD — do that repairing by promoting the growth of nerve cell branches that receive information, called dendrites (SN: 11/17/20). The behavior might explain the drugs’ positive outcomes in research. But how they trigger cell growth was a mystery. It was already known that, in cortical neurons, psychedelics activate a certain protein that receives signals and gives instructions to cells. This protein, called the 5-HT2A receptor, is also stimulated by serotonin, a chemical made by the body and implicated in mood. But a study in 2018 determined that serotonin doesn’t make these neurons grow. That finding “was really leaving us scratching our heads,” says chemical neuroscientist David Olson, director of the Institute for Psychedelics and Neurotherapeutics at the University of California, Davis. © Society for Science & the Public 2000–2023.

Keyword: Drug Abuse; Depression
Link ID: 28673 - Posted: 02.18.2023

Jane Clinton For those of us who struggle to leave our beds in the winter, taunts of “lazy” could well be misplaced. New research suggests that while humans do not hibernate, we may need more sleep during the colder months. Analysis of people undergoing sleep studies found that people get more REM (rapid eye movement) sleep in the winter. While total sleep time appeared to be about an hour longer in the winter than the summer, this result was not considered statistically significant. However, REM sleep – known to be directly linked to the circadian clock, which is affected by changing light – was 30 minutes longer in the winter than in summer. The research suggests that even in an urban population experiencing disrupted sleep, humans experience longer REM sleep in winter than summer and less deep sleep in autumn. Researchers say if the study’s findings can be replicated in people with healthy sleep, this would provide the first evidence for a need to adjust sleep habits to season – perhaps by going to sleep earlier in the darker and colder months. Dr Dieter Kunz, corresponding author of the study, based at the Clinic for Sleep & Chronomedicine at the St Hedwig hospital, Germany, said: “Seasonality is ubiquitous in any living being on this planet. “Even though we still perform unchanged over the winter, human physiology is down-regulated, with a sensation of ‘running-on-empty’ in February or March. “In general, societies need to adjust sleep habits including length and timing to season, or adjust school and working schedules to seasonal sleep needs.”

Keyword: Biological Rhythms; Sleep
Link ID: 28672 - Posted: 02.18.2023

By Sheryl Gay Stolberg and Ellen Barry Lynn Rivers, a Democrat from Michigan, opened up about her diagnosis with bipolar disorder during a radio call-in show when she first ran for Congress. Her opponents had been hinting she had mental health problems. She decided, spur of the moment, to let it out. “Finally, I just said, ‘Are you asking me if I have depression? Yes, and so do thousands and millions of other people,’” she recalled. “I was like, ‘OK, here we go. The ball is thrown at you, just hit it.’ And so I did.” That was 1994. Ms. Rivers was elected, despite a Republican tidal wave, and served four terms. Now another Democrat, Senator John Fetterman of Pennsylvania, has announced that he has entered a hospital to be treated for clinical depression. Politicians of both parties are praising him for his openness. Mental health experts say he is a powerful symbol — especially for men, who are less likely to seek treatment for depression and suffer higher rates of suicide. Yet the stigma around mental illness remains strong — especially in politics, where questions about temperament can determine a candidate’s electability. Mr. Fetterman and others face a continuing challenge: How much do they really want to say? “We’ve come a long way; people are willing to say they have a diagnosis or that they’re going to therapy,” said Patrick J. Kennedy, a scion of the political Kennedy family, who disclosed his treatment for bipolar disorder and drug abuse when he was a congressman from Rhode Island. “But we’re still not in a place where people are comfortable saying any more than that. And really the question with Senator Fetterman is: How much is he going to disclose?” Clinical depression, also called major depression, is a severe form of the disease. Symptoms may include feelings of sadness, hopelessness or guilt; angry outbursts; loss of pleasure in ordinary activities; fatigue; anxiety; reduced appetite; and thoughts of suicide. In recent years, there have been great strides in treatment. © 2023 The New York Times Company

Keyword: Depression; Stroke
Link ID: 28671 - Posted: 02.18.2023

By Laura Sanders You’d be forgiven for thinking that depression has a simple explanation. The same mantra — that the mood disorder comes from a chemical imbalance in the brain — is repeated in doctors’ offices, medical textbooks and pharmaceutical advertisements. Those ads tell us that depression can be eased by tweaking the chemicals that are off-kilter in the brain. The only problem — and it’s a big one — is that this explanation isn’t true. The phrase “chemical imbalance” is too vague to be true or false; it doesn’t mean much of anything when it comes to the brain and all its complexity. Serotonin, the chemical messenger often tied to depression, is not the one key thing that explains depression. The same goes for other brain chemicals. The hard truth is that despite decades of sophisticated research, we still don’t understand what depression is. There are no clear descriptions of it, and no obvious signs of it in the brain or blood. The reasons we’re in this position are as complex as the disease itself. Commonly used measures of depression, created decades ago, neglect some important symptoms and overemphasize others, particularly among certain groups of people. Even if depression could be measured perfectly, the disorder exists amid myriad levels of complexity, from biological confluences of minuscule molecules in the brain all the way out to the influences of the world at large. Countless combinations of genetics, personality, history and life circumstances may all conspire to create the disorder in any one person. No wonder the science is stuck. So here, up front, is your fair warning: There will be no satisfying wrap-up at the end of this story. You will not come away with a scientific explanation for depression, because one does not exist. But there is a way forward for depression researchers, Aftab says. It requires grappling with nuances, complexity and imperfect data. © Society for Science & the Public 2000–2023.

Keyword: Depression
Link ID: 28670 - Posted: 02.15.2023

By Veronique Greenwood It is the rare person who likes hearing their own voice on a recording. It sounds fake, somehow — like it belongs to someone else. For neuroscientists, that quality of otherness is more than a curiosity. Many mysteries remain about the origins of hallucinations, but one hypothesis suggests that when people hear voices, they are hearing their own thoughts disguised as another person’s by a quirk of the brain. Scientists would like to understand what parts of the brain allow us to recognize ourselves speaking, but studying this using recordings of people’s own voices has proved tricky. When we talk, we not only hear our voice with our ears, but on some level we feel it as the sound vibrations travel through the bones of the skull. A study published Wednesday in the journal Royal Society Open Science attempted a workaround. A team of researchers investigated whether people could more accurately recognize their voices if they wore bone-conduction headphones, which transmit sound via vibration. They found that sending a recording through the facial bones made it easier for people to tell their voices apart from those of strangers, suggesting that this technology provides a better way to study how we can tell when we are speaking. That is a potentially important step in understanding the origins of hallucinated voices. Recordings of our voices tend to sound higher than we expect, said Pavo Orepic, a postdoctoral researcher at the Swiss Federal Institute of Technology who led the study. The vibration of the skull makes your voice sound deeper to yourself than to a listener. But even adjusting recordings so they sound lower doesn’t recreate the experience of hearing your own voice. As an alternative, the team tried using bone-conduction headphones, which are commercially available and often rest on a listener’s cheekbones just in front of the ear. © 2023 The New York Times Company

Keyword: Schizophrenia; Hearing
Link ID: 28669 - Posted: 02.15.2023

By Allison Whitten The neocortex stands out as a stunning achievement of biological evolution. All mammals have this swath of tissue covering their brain, and the six layers of densely packed neurons within it handle the sophisticated computations and associations that produce cognitive prowess. Since no animals other than mammals have a neocortex, scientists have wondered how such a complex brain region evolved. The brains of reptiles seemed to offer a clue. Not only are reptiles the closest living relatives of mammals, but their brains have a three-layered structure called a dorsal ventricular ridge, or DVR, with functional similarities to the neocortex. For more than 50 years, some evolutionary neuroscientists have argued that the neocortex and the DVR were both derived from a more primitive feature in an ancestor shared by mammals and reptiles. Now, however, by analyzing molecular details invisible to the human eye, scientists have refuted that view. By looking at patterns of gene expression in individual brain cells, researchers at Columbia University showed that despite the anatomical similarities, the neocortex in mammals and the DVR in reptiles are unrelated. Instead, mammals seem to have evolved the neocortex as an entirely new brain region, one built without a trace of what came before it. The neocortex is composed of new types of neurons that seem to have no precedent in ancestral animals. The paper describing this work, which was led by the evolutionary and developmental biologist Maria Antonietta Tosches, was published last September in Science. This process of evolutionary innovation in the brain isn’t limited to the creation of new parts. Other work by Tosches and her colleagues in the same issue of Science showed that even seemingly ancient brain regions are continuing to evolve by getting rewired with new types of cells. The discovery that gene expression can reveal these kinds of important distinctions between neurons is also prompting researchers to rethink how they define some brain regions and to reassess whether some animals might have more complex brains than they thought. All Rights Reserved © 2023

Keyword: Development of the Brain; Evolution
Link ID: 28668 - Posted: 02.15.2023

By Stephani Sutherland Tara Ghormley has always been an overachiever. She finished at the top of her class in high school, graduated summa cum laude from college and earned top honors in veterinary school. She went on to complete a rigorous training program and build a successful career as a veterinary internal medicine specialist. But in March 2020 she got infected with the SARS-CoV-2 virus—just the 24th case in the small, coastal central California town she lived in at the time, near the site of an early outbreak in the COVID pandemic. “I could have done without being first at this,” she says. Almost three years after apparently clearing the virus from her body, Ghormley is still suffering. She gets exhausted quickly, her heartbeat suddenly races, and she goes through periods where she can't concentrate or think clearly. Ghormley and her husband, who have relocated to a Los Angeles suburb, once spent their free time visiting their “happiest place on Earth”—Disneyland—but her health prevented that for more than a year. She still spends most of her days off resting in the dark or going to her many doctors' appointments. Her early infection and ongoing symptoms make her one of the first people in the country with “long COVID,” a condition where symptoms persist for at least three months after the infection and can last for years. The syndrome is known by medical professionals as postacute sequelae of COVID-19, or PASC. People with long COVID have symptoms such as pain, extreme fatigue and “brain fog,” or difficulty concentrating or remembering things. As of February 2022, the syndrome was estimated to affect about 16 million adults in the U.S. and had forced between two million and four million Americans out of the workforce, many of whom have yet to return. Long COVID often arises in otherwise healthy young people, and it can follow even a mild initial infection. The risk appears at least slightly higher in people who were hospitalized for COVID and in older adults (who end up in the hospital more often). Women and those at socioeconomic disadvantage also face higher risk, as do people who smoke, are obese, or have any of an array of health conditions, particularly autoimmune disease. Vaccination appears to reduce the danger but does not entirely prevent long COVID.

Keyword: Attention; Learning & Memory
Link ID: 28667 - Posted: 02.15.2023

By Ted Alcorn Ever wake up regretting the last round of drinks from the previous night? There’s a medicine that might help. A recent study adds to the evidence that people who binge-drink may benefit from taking a dose of the medication naltrexone before consuming alcohol, a finding that may be welcomed now that alcohol-related deaths in the United States have surpassed 140,000 a year. Nearly half of American drinkers reported bingeing, defined as more than four drinks in a sitting for men and more than three for women, in the previous month, according to a U.S. government health survey. Some may view binge-drinking as harmless because the habit is widespread and a low percentage of binge drinkers are dependent on alcohol, according to experts. But it is considered a major risk factor for alcohol-related illness and injuries, and it heightens the possibility that an individual will develop an alcohol disorder. In the study, which was published in December in the American Journal of Psychiatry, 120 men who wanted to reduce bingeing but were not severely dependent on alcohol were given naltrexone to take whenever they felt a craving for alcohol or anticipated a period of heavy drinking. Naltrexone, which blocks endorphins and reduces the euphoria of intoxication, was approved in the United States for the treatment of alcohol dependence nearly 30 years ago. But it is typically prescribed for patients with more severe alcohol disorders to take daily to abstain from drinking. The new study’s targeted approach, in which patients were advised to take the pill one hour before they expected to drink, is less common, although studies going back decades have also demonstrated the effectiveness of the as-needed dosing method. © 2023 The New York Times Company

Keyword: Drug Abuse
Link ID: 28666 - Posted: 02.15.2023

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

Keyword: Epilepsy
Link ID: 28665 - Posted: 02.15.2023

By Erin Garcia de Jesús A female giraffe has a great Valentine’s Day gift for potential mates: urine. Distinctive anatomy helps male giraffes get a taste for whether a female is ready to mate, animal behaviorists Lynette and Benjamin Hart report January 19 in Animals. A pheromone-detecting organ in giraffes has a stronger connection to the mouth than the nose, the researchers found. That’s why males scope out which females to mate with by sticking their tongues in a urine stream. Animals such as male gazelles will lick fresh urine on the ground to track if females are ready to mate. But giraffes’ long necks and heavy heads make bending over to investigate urine on the ground an unstable and vulnerable position, says Lynette Hart, of the University of California, Davis. The researchers observed giraffes (Giraffa giraffa angolensis) in Etosha National Park in Namibia in 1994, 2002 and 2004. Bull giraffes nudged or kicked the female to ask her to pee. If she was a willing participant, she urinated for a few seconds, while the male took a sip. Then the male curled his lip and inhaled with his mouth, a behavior called a flehmen response, to pull the female’s scent into two openings on the roof of the mouth. From the mouth, the scent travels to the vomeronasal organ, or VNO, which detects pheromones. The Harts say they never saw a giraffe investigate urine on the ground. Unlike many other mammals, giraffes have a stronger oral connection — via a duct — to the VNO, than a nasal one, examinations of preserved giraffe specimens showed. One possible explanation for the difference could be that a VNO-nose link helps animals that breed at specific times of the year detect seasonal plants, says Benjamin Hart, a veterinarian also at the University of California, Davis. But giraffes can mate any time of year, so the nasal connection may not matter as much. © Society for Science & the Public 2000–2023.

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 28664 - Posted: 02.15.2023

By Erin Garcia de Jesús Forget screwdrivers or drills. A stick and a straw make for a great cockatoo tool kit. Some Goffin’s cockatoos (Cacatua goffiniana) know whether they need to have more than one tool in claw to topple an out-of-reach cashew, researchers report February 10 in Current Biology. By recognizing that two items are necessary to access the snack, the birds join chimpanzees as the only nonhuman animals known to use tools as a set. The study is a fascinating example of what cockatoos are capable of, says Anne Clark, a behavioral ecologist at Binghamton University in New York, who was not involved in the study. A mental awareness that people often attribute to our close primate relatives can also pop up elsewhere in the animal kingdom. A variety of animals including crows and otters use tools but don’t deploy multiple objects together as a kit (SN: 9/14/16; SN: 3/21/17). Chimpanzees from the Republic of Congo’s Noubalé-Ndoki National Park, on the other hand, recognize the need for both a sharp stick to break into termite mounds and a fishing stick to scoop up an insect feast (SN: 10/19/04). Researchers knew wild cockatoos could use three different sticks to break open fruit in their native range of Indonesia. But it was unclear whether the birds might recognize the sticks as a set or instead as a chain of single tools that became necessary as new problems arose, says evolutionary biologist Antonio Osuna Mascaró of the University of Veterinary Medicine Vienna. © Society for Science & the Public 2000–2023.

Keyword: Learning & Memory; Evolution
Link ID: 28663 - Posted: 02.11.2023