By Judith Warner Dr. Benjamin Rush, the 18th-century doctor who is often called the “father” of American psychiatry, held the racist belief that Black skin was the result of a mild form of leprosy. He called the condition “negritude.” His onetime apprentice, Dr. Samuel Cartwright, spread the falsehood throughout the antebellum South that enslaved people who experienced an unyielding desire to be free were in the grip of a mental illness he called “drapetomania,” or “the disease causing Negroes to run away.” In the late 20th century, psychiatry’s rank and file became a receptive audience for drug makers who were willing to tap into racist fears about urban crime and social unrest. (“Assaultive and belligerent?” read an ad that featured a Black man with a raised fist that appeared in the “Archives of General Psychiatry” in 1974. “Cooperation often begins with Haldol.”) Now the American Psychiatric Association, which featured Rush’s image on its logo until 2015, is confronting that painful history and trying to make amends. In January, the 176-year-old group issued its first-ever apology for its racist past. Acknowledging “appalling past actions” on the part of the profession, its governing board committed the association to “identifying, understanding, and rectifying our past injustices,” and pledged to institute “anti-racist practices” aimed at ending the inequities of the past in care, research, education and leadership. This weekend, the A.P.A. is devoting its annual meeting to the theme of equity. Over the course of the three-day virtual gathering of as many as 10,000 participants, the group will present the results of its yearlong effort to educate its 37,000 mostly white members about the psychologically toxic effects of racism, both in their profession and in the lives of their patients. © 2021 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 27797 - Posted: 05.01.2021

Jon Hamilton An experimental drug intended for Alzheimer's patients seems to improve both language and learning in adults with Fragile X syndrome. The drug, called BPN14770, increased cognitive scores by about 10% in 30 adult males after 12 weeks, a team reports in the journal Nature Medicine. That is enough to change the lives of many people with Fragile X, says Mark Gurney, CEO of Tetra Therapeutics, developer of the medicine. "People with Fragile X with an IQ of 40 are typically living with their parents or in an institutional setting," Gurney says. "With an IQ of 50, in some cases they're able to ride the bus, they're able to hold a job with some assistance and they're able to function better in their community." But it will take a much larger study to know whether the drug is as good as it seems, says Mark Bear, Picower professor of neuroscience at the Massachusetts Institute of Technology. "This study is certainly not definitive, but it's encouraging," he says. Fragile X syndrome is a genetic disorder that affects about 1 in 4,000 males and a smaller proportion of females. It is the most common inherited cause of intellectual disabilities and autism. The idea of treating Fragile X with an Alzheimer's drug came from Gurney after he learned that both conditions affect a substance called cyclic AMP that helps transmit messages inside cells. © 2021 npr

Keyword: Alzheimers; Development of the Brain
Link ID: 27796 - Posted: 05.01.2021

Enhancing the brain’s lymphatic system when administering immunotherapies may lead to better clinical outcomes for Alzheimer’s disease patients, according to a new study in mice. Results published April 28 in Nature suggest that treatments such as the immunotherapies BAN2401 or aducanumab might be more effective when the brain’s lymphatic system can better drain the amyloid-beta protein that accumulates in the brains of those living with Alzheimer’s. Major funding for the research was provided by the National Institute on Aging (NIA), part of the National Institutes of Health, and all study data is now freely available to the broader scientific community. “A broad range of research on immunotherapies in development to treat Alzheimer’s by targeting amyloid-beta has not to date demonstrated consistent results,” said NIA Director Richard J. Hodes, M.D. “While this study’s findings require further confirmation, the link it has identified between a well-functioning lymphatic system in the brain and the ability to reduce amyloid-beta accumulation may be a significant step forward in pursuing this class of therapeutics.” Abnormal buildup of amyloid-beta is one hallmark of Alzheimer’s disease. The brain’s lymphatic drainage system, which removes cellular debris and other waste, plays an important part in that accumulation. A 2018 NIA-supported study showed a link between impaired lymphatic vessels and increased amyloid-beta deposits in the brains of aging mice, suggesting these vessels could play a role in age-related cognitive decline and Alzheimer’s. The lymphatic system is made up of vessels which run alongside blood vessels and which carry immune cells and waste to lymph nodes. Lymphatic vessels extend into the brain’s meninges, which are membranes that surround the brain and spinal cord.

Keyword: Alzheimers; Sleep
Link ID: 27795 - Posted: 05.01.2021

By Noah Hutton Twelve years ago, when I graduated college, I was well aware of the Silicon Valley hype machine, but I considered the salesmanship of private tech companies a world away from objective truths about human biology I had been taught in neuroscience classes. At the time, I saw the neuroscientist Henry Markram proclaim in a TED talk that he had figured out a way to simulate an entire human brain on supercomputers within 10 years. This computer-simulated organ would allow scientists to instantly and noninvasively test new treatments for disorders and diseases, moving us from research that depends on animal experimentation and delicate interventions on living people to an “in silico” approach to neuroscience. My 22-year-old mind didn’t clock this as an overhyped proposal. Instead, it felt exciting and daring, the kind of moment that transforms a distant scientific pipe dream into a suddenly tangible goal and motivates funders and fellow researchers to think bigger. And so I began a 10-year documentary project following Markram and his Blue Brain Project, with the start of the film coinciding with the beginning of an era of big neuroscience where the humming black boxes produced by Silicon Valley came to be seen as the great new hope for making sense of the black boxes between our ears. My decade-long journey documenting Markram’s vision has no clear answers except perhaps one: that flashy presentations and sheer ambition are poor indicators of success when it comes to understanding the complex biological mechanisms of brains. Today, as we bear witness to a game of Pong being mind-controlled by a monkey as part of a typically bombastic demonstration by Elon Musk’s start-up Neuralink, there is more of a need than ever to unwind the cycles of hype in order to grapple with what the future of brain technology and neuroscience have in store for humanity. © 2021 Scientific American

Keyword: Brain imaging; Robotics
Link ID: 27794 - Posted: 05.01.2021

by Angie Voyles Askham A brain circuit that connects the amygdala to the hypothalamus is essential for deriving pleasure from social interactions, according to a new study in mice. Alterations in this circuit may help explain why autistic people tend to have less social motivation than their non-autistic peers. The release of the neurotransmitter dopamine into the striatum prompts the rewarding feelings that come from stimuli such as food or sex, previous research shows. But it was unclear whether all social reward is processed in that same circuit, or if it occurs in a separate brain area that later links up with the striatum, the brain’s reward center, says lead researcher Weizhe Hong, associate professor of neurobiology and biological chemistry at the University of California, Los Angeles. Hong and his colleagues trained mice on a social test and then altered activity in the animals’ medial amygdala, which has been linked to the regulation of social behaviors. Cells in the area carry information about social reward to the medial preoptic area of the hypothalamus, the team found. And activation of this circuit prompts the release of dopamine in the striatum. “It’s filling a gap that existed” in the field, says Jessica Walsh, assistant professor of pharmacology at the University of North Carolina at Chapel Hill, who was not involved in the study. © 2021 Simons Foundation

Keyword: Autism; Drug Abuse
Link ID: 27793 - Posted: 05.01.2021

By Laura Sanders For more than a year now, scientists have been racing to understand how the mysterious new virus that causes COVID-19 damages not only our bodies, but also our brains. Early in the pandemic, some infected people noticed a curious symptom: the loss of smell. Reports of other brain-related symptoms followed: headaches, confusion, hallucinations and delirium. Some infections were accompanied by depression, anxiety and sleep problems. Recent studies suggest that leaky blood vessels and inflammation are somehow involved in these symptoms. But many basic questions remain unanswered about the virus, which has infected more than 145 million people worldwide. Researchers are still trying to figure out how many people experience these psychiatric or neurological problems, who is most at risk, and how long such symptoms might last. And details remain unclear about how the pandemic-causing virus, called SARS-CoV-2, exerts its effects. “We still haven’t established what this virus does in the brain,” says Elyse Singer, a neurologist at the University of California, Los Angeles. There are probably many answers, she says. “It’s going to take us years to tease this apart.” Getting the numbers For now, some scientists are focusing on the basics, including how many people experience these sorts of brain-related problems after COVID-19. © Society for Science & the Public 2000–2021.

Keyword: Alzheimers; Depression
Link ID: 27792 - Posted: 04.28.2021

By Christine Kenneally The first thing that Rita Leggett saw when she regained consciousness was a pair of piercing blue eyes peering curiously into hers. “I know you, don’t I?” she said. The man with the blue eyes replied, “Yes, you do.” But he didn’t say anything else, and for a while Leggett just wondered and stared. Then it came to her: “You’re my surgeon!” It was November, 2010, and Leggett had just undergone neurosurgery at the Royal Melbourne Hospital. She recalled a surge of loneliness as she waited alone in a hotel room the night before the operation and the fear she felt when she entered the operating room. She’d worried about the surgeon cutting off her waist-length hair. What am I doing in here? she’d thought. But just before the anesthetic took hold, she recalled, she had said to herself, “I deserve this.” Leggett was forty-nine years old and had suffered from epilepsy since she was born. During the operation, her surgeon, Andrew Morokoff, had placed an experimental device inside her skull, part of a brain-computer interface that, it was hoped, would be able to predict when she was about to have a seizure. The device, developed by a Seattle company called NeuroVista, had entered a trial stage known in medical research as “first in human.” A research team drawn from three prominent epilepsy centers based in Melbourne had selected fifteen patients to test the device. Leggett was Patient 14. © 2021 Condé Nast.

Keyword: Robotics; Epilepsy
Link ID: 27791 - Posted: 04.28.2021

Michael Marshall In her laboratory in Barcelona, Spain, Miki Ebisuya has built a clock without cogs, springs or numbers. This clock doesn’t tick. It is made of genes and proteins, and it keeps time in a layer of cells that Ebisuya’s team has grown in its lab. This biological clock is tiny, but it could help to explain some of the most conspicuous differences between animal species. Animal cells bustle with activity, and the pace varies between species. In all observed instances, mouse cells run faster than human cells, which tick faster than whale cells. These differences affect how big an animal gets, how its parts are arranged and perhaps even how long it will live. But biologists have long wondered what cellular timekeepers control these speeds, and why they vary. A wave of research is starting to yield answers for one of the many clocks that control the workings of cells. There is a clock in early embryos that beats out a regular rhythm by activating and deactivating genes. This ‘segmentation clock’ creates repeating body segments such as the vertebrae in our spines. This is the timepiece that Ebisuya has made in her lab. “I’m interested in biological time,” says Ebisuya, a developmental biologist at the European Molecular Biology Laboratory Barcelona. “But lifespan or gestation period, they are too long for me to study.” The swift speed of the segmentation clock makes it an ideal model system, she says. © 2021 Springer Nature Limited

Keyword: Development of the Brain; Evolution
Link ID: 27790 - Posted: 04.28.2021

by Jessica Jiménez, Mark Zylka Mice and rats typically give birth to 6 to 12 animals per litter. Some scientists treat this as a benefit, because a large number of animals can be produced with a small number of matings. In reality, though, this is of no benefit at all, especially when you consider a fact that is well known in the toxicology field: Animals within a litter are more similar to one another than animals between litters. Herein lies what is known as the ‘litter effect.’ Anyone who uses multiple animals from a small number of litters to increase sample size is making a serious mistake. The similarities within individual litters will heavily skew the results. Our goal in writing this article, and an accompanying peer-reviewed paper on this topic, is to raise awareness about the litter effect and to encourage researchers who study neurodevelopmental conditions to control for it in future work. Like many scientists who use rodents to study autism and related conditions, we were oblivious to the litter effect and its impact on research. However, we now recognize that it is essential to control for the litter effect whenever a rodent autism model is studied, be it a mouse with a gene mutation or an environmental exposure. It is essential because the litter effect can lead to erroneous conclusions that negatively influence the rigor and reproducibility of scientific research. Indeed, false positives, or the incorrect identification of a significant effect, increase as fewer litters are sampled. Conversely, litter-to-litter variation adds ‘noise’ to the data that can mask true treatment or genetic effects. This is concerning because most phenotypes associated with rodent models of autism are remarkably small, and they are often difficult to reproduce between labs. © 2021 Simons Foundation

Keyword: Development of the Brain; Sexual Behavior
Link ID: 27789 - Posted: 04.28.2021

The government of New Brunswick says there are now 47 cases of a mysterious neurological disease, for which experts are still trying to figure out a source. As of last Thursday, there have been 37 confirmed and 10 suspected cases of "a neurological syndrome of unknown cause," Bruce Macfarlane, spokesperson for the Department of Health, said in an email Monday. That brings the number of cases up from 44. The province last reported a new case in early April. There have been six deaths caused by the disease, with no new deaths reported Monday. Macfarlane said the province is collaborating with local and national subject matter experts and health-care providers to investigate the individuals showing signs and symptoms of the syndrome. "At this time, the investigation is active and ongoing to determine if there are similarities among the reported cases that can identify potential causes for this syndrome, and to help identify possible strategies for prevention. "The investigation team is exploring all potential causes including food, environmental and animal exposures." Macfarlane said most of the cases are in people who were living in areas around Moncton and on the Acadian Peninsula. "However, it is unknown at this stage of our investigation whether geographic area is linked to the neurological condition and related symptoms" he said. The disease cluster was first reported on in March, when Radio-Canada obtained a memo from Public Health to medical professionals. ©2021 CBC/Radio-Canada.

Keyword: Alzheimers; Neurotoxins
Link ID: 27788 - Posted: 04.28.2021

By Kathiann Kowalski On most mornings, Jeremy D. Brown eats an avocado. But first, he gives it a little squeeze. A ripe avocado will yield to that pressure, but not too much. Brown also gauges the fruit’s weight in his hand and feels the waxy skin, with its bumps and ridges. “I can’t imagine not having the sense of touch to be able to do something as simple as judging the ripeness of that avocado,” says Brown, a mechanical engineer who studies haptic feedback — how information is gained or transmitted through touch — at Johns Hopkins University. Many of us have thought about touch more than usual during the COVID-19 pandemic. Hugs and high fives rarely happen outside of the immediate household these days. A surge in online shopping has meant fewer chances to touch things before buying. And many people have skipped travel, such as visits to the beach where they might sift sand through their fingers. A lot goes into each of those actions. “Anytime we touch anything, our perceptual experience is the product of the activity of thousands of nerve fibers and millions of neurons in the brain,” says neuroscientist Sliman Bensmaia of the University of Chicago. The body’s natural sense of touch is remarkably complex. Nerve receptors detect cues about pressure, shape, motion, texture, temperature and more. Those cues cause patterns of neural activity, which the central nervous system interprets so we can tell if something is smooth or rough, wet or dry, moving or still. © Society for Science & the Public 2000–2021.

Keyword: Pain & Touch; Robotics
Link ID: 27787 - Posted: 04.24.2021

By Pam Belluck Could getting too little sleep increase your chances of developing dementia? For years, researchers have pondered this and other questions about how sleep relates to cognitive decline. Answers have been elusive because it is hard to know if insufficient sleep is a symptom of the brain changes that underlie dementia — or if it can actually help cause those changes. Now, a large new study reports some of the most persuasive findings yet to suggest that people who don’t get enough sleep in their 50s and 60s may be more likely to develop dementia when they are older. The research, published Tuesday in the journal Nature Communications, has limitations but also several strengths. It followed nearly 8,000 people in Britain for about 25 years, beginning when they were 50 years old. It found that those who consistently reported sleeping six hours or less on an average weeknight were about 30 percent more likely than people who regularly got seven hours sleep (defined as “normal” sleep in the study) to be diagnosed with dementia nearly three decades later. “It would be really unlikely that almost three decades earlier, this sleep was a symptom of dementia, so it’s a great study in providing strong evidence that sleep is really a risk factor,” said Dr. Kristine Yaffe, a professor of neurology and psychiatry at the University of California, San Francisco, who was not involved in the study. Pre-dementia brain changes like accumulations of proteins associated with Alzheimer’s are known to begin about 15 to 20 years before people exhibit memory and thinking problems, so sleep patterns within that time frame could be considered an emerging effect of the disease. That has posed a “chicken or egg question of which comes first, the sleep problem or the pathology,” said Dr. Erik Musiek, a neurologist and co-director of the Center on Biological Rhythms and Sleep at Washington University in St. Louis, who was not involved in the new research. © 2021 The New York Times Company

Keyword: Sleep; Alzheimers
Link ID: 27786 - Posted: 04.24.2021

By Virginia Morell Like members of a street gang, male dolphins summon their buddies when it comes time to raid and pillage—or, in their case, to capture and defend females in heat. A new study reveals they do this by learning the “names,” or signature whistles, of their closest allies—sometimes more than a dozen animals—and remembering who consistently cooperated with them in the past. The findings indicate dolphins have a concept of team membership—previously seen only in humans—and may help reveal how they maintain such intricate and tight-knit societies. “It is a ground-breaking study,” says Luke Rendell, a behavioral ecologist at the University of St. Andrews who was not involved with the research. The work adds evidence to the idea that dolphins evolved large brains to navigate their complex social environments. Male dolphins typically cooperate as a pair or trio, in what researchers call a “first-order alliance.” These small groups work together to find and corral a fertile female. Males also cooperate in second-order alliances comprised of as many as 14 dolphins; these defend against rival groups attempting to steal the female. Some second-order alliances join together in even larger third-order alliances, providing males in these groups with even better chances of having allies nearby should rivals attack. © 2021 American Association for the Advancement of Science

Keyword: Animal Communication; Language
Link ID: 27785 - Posted: 04.24.2021

Lise Eliot Everyone knows the difference between male and female brains. One is chatty and a little nervous, but never forgets and takes good care of others. The other is calmer, albeit more impulsive, but can tune out gossip to get the job done. These are stereotypes, of course, but they hold surprising sway over the way actual brain science is designed and interpreted. Since the dawn of MRI, neuroscientists have worked ceaselessly to find differences between men’s and women’s brains. This research attracts lots of attention because it’s just so easy to try to link any particular brain finding to some gender difference in behavior. But as a neuroscientist long experienced in the field, I recently completed a painstaking analysis of 30 years of research on human brain sex differences. And what I found, with the help of excellent collaborators, is that virtually none of these claims has proven reliable. Except for the simple difference in size, there are no meaningful differences between men’s and women’s brain structure or activity that hold up across diverse populations. Nor do any of the alleged brain differences actually explain the familiar but modest differences in personality and abilities between men and women. © 2010–2021, The Conversation US, Inc.

Keyword: Sexual Behavior; Brain imaging
Link ID: 27784 - Posted: 04.24.2021

by Angie Voyles Askham A dearth of insulation around neuronal projections may explain why some parts of the cerebral cortex can appear thicker in brain scans of autistic people than in those of non-autistic people, according to a new study. Magnetic resonance imaging (MRI) studies show that some autistic children have bigger brains than their non-autistic peers, with much of the overgrowth occurring in the cerebral cortex. The reason for this difference remains unclear, but it seems to reflect an apparent excess of gray matter, which consists of neuronal cell bodies, relative to white matter, composed of neuronal projections. Newly developed neurons in the brains of autistic people may have trouble migrating to the proper place, some researchers have suggested, which could blur the boundary between gray and white matter in some regions and cause the gray matter to look thicker on an MRI scan. But higher levels of myelin, the insulation that surrounds neuronal projections, in non-autistic people could also skew these measures, says lead researcher of the new work, Mallar Chakravarty, associate professor of psychiatry at McGill University in Montreal. Myelin appears brighter on an MRI scan than other tissue, so an abundance of it near the boundary between gray and white matter could make the gray matter appear thinner, he says. © 2021 Simons Foundation

Keyword: Autism; Glia
Link ID: 27783 - Posted: 04.24.2021

Johnjoe McFadden Some 2,700 years ago in the ancient city of Sam’al, in what is now modern Turkey, an elderly servant of the king sits in a corner of his house and contemplates the nature of his soul. His name is Katumuwa. He stares at a basalt stele made for him, featuring his own graven portrait together with an inscription in ancient Aramaic. It instructs his family, when he dies, to celebrate ‘a feast at this chamber: a bull for Hadad harpatalli and a ram for Nik-arawas of the hunters and a ram for Shamash, and a ram for Hadad of the vineyards, and a ram for Kubaba, and a ram for my soul that is in this stele.’ Katumuwa believed that he had built a durable stone receptacle for his soul after death. This stele might be one of the earliest written records of dualism: the belief that our conscious mind is located in an immaterial soul or spirit, distinct from the matter of the body. More than 2 millennia later, I was also contemplating the nature of the soul, as my son lay propped up on a hospital gurney. He was undertaking an electroencephalogram (EEG), a test that detects electrical activity in the brain, for a condition that fortunately turned out to be benign. As I watched the irregular wavy lines march across the screen, with spikes provoked by his perceptions of events such as the banging of a door, I wondered at the nature of the consciousness that generated those signals. Just how do the atoms and molecules that make up the neurons in our brain – not so different to the bits of matter in Katumwa’s inert stele or the steel barriers on my son’s hospital bed – manage to generate human awareness and the power of thought? In answering that longstanding question, most neurobiologists today would point to the information-processing performed by brain neurons. For both Katumuwa and my son, this would begin as soon as light and sound reached their eyes and ears, stimulating their neurons to fire in response to different aspects of their environment. For Katumuwa, perhaps, this might have been the pinecone or comb that his likeness was holding on the stele; for my son, the beeps from the machine or the movement of the clock on the wall. © Aeon Media Group Ltd. 2012-2021

Keyword: Consciousness; Attention
Link ID: 27782 - Posted: 04.21.2021

By Emily Anthes Male tanagers are meant to be noticed. Many species of the small, tropical bird sport deep black feathers and splashes of eye-catching color — electric yellows, traffic-cone oranges and nearly neon scarlets. To achieve this flashiness, the birds must spend time and energy foraging for, and metabolizing, plants that contain special color pigments, which make their way into the feathers. A vibrantly colored male is thus sending an “honest signal,” many scientists have long theorized: He is alerting nearby females that he has a good diet, is in good health and would make a worthy mate. But some birds may be guilty of false advertising, a new study suggests. Male tanagers have microstructures in their feathers that enhance their colors, researchers reported Wednesday in the journal Scientific Reports. These microstructures, like evolution’s own Instagram filters, may make the males seem as if they are more attractive than they truly are. “Many male birds are colorful not just because they’re honestly signaling their quality, but because they’re trying to get chosen,” said Dakota McCoy, a doctoral student at Harvard University who conducted the research as part of her dissertation. “This is basically experimental evidence that whenever there’s a high-stakes test in life, it’s worth your while to cheat a little bit.” The new study is an important contribution to the longstanding debate over how, and why, brightly colored feathers evolved in birds, said Geoffrey Hill, an ornithologist and evolutionary ecologist at Auburn University. “Scientists have spent the last 150 years since Darwin and Wallace trying to understand ornaments in animals and especially colors in birds,” he said. “And this is the kind of original approach that helps us.” © 2021 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 27781 - Posted: 04.21.2021

David Cox When John Abraham began to lose his mind in late 2019, his family immediately feared the worst. Abraham had enjoyed robust health throughout retirement, but now at 80 he suddenly found himself struggling to finish sentences. “I would be talking to people, and all of a sudden the final word wouldn’t come to mind,” he remembers. “I assumed this was simply a feature of ageing, and I was finding ways of getting around it.” But within weeks, further erratic behaviours started to develop. Abraham’s family recall him often falling asleep mid-conversation, he would sometimes shout out bizarre comments in public, and during the night he would wake up every 15 minutes, sometimes hallucinating. Patients can go from being in a nursing home, unable to communicate, to returning to work To his son Steve, the diagnosis seemed inevitable, one which all families dread. “I was convinced my dad had dementia,” he says. “What I couldn’t believe was the speed at which it was all happening. It was like dementia on steroids.” Dementia is not just one disease – it has more than 200 different subtypes. Over the past decade neurologists have become increasingly interested in one particular subtype, known as autoimmune dementia. In this condition, the symptoms of memory loss and confusion are the result of brain inflammation caused by rogue antibodies – known as autoantibodies – binding to the neuronal tissue, rather than an underlying neurodegenerative disease. Crucially this means that unlike almost all other forms of dementia, in some cases it can be cured, andspecialist neurologists have become increasingly adept at both spotting and treating it. © 2021 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 27780 - Posted: 04.21.2021

By Nambi Ndugga and Austin Frakt American deaths from misuse of substances, including alcohol, have increased over the past two decades, but not uniformly across various demographic groups. Overall rates of alcohol abuse and related deaths have consistently and significantly increased for white non-Hispanic Americans, while Black Americans have experienced a much slower and less significant incline, and some other groups have had declines. More recently, alcohol use has been up during the pandemic, with one study showing a greater increase in misuse among women than among men. (For men, heavy drinking is considered more than four drinks per day and 14 drinks per week, and for women, more than three drinks per day and seven drinks per week, according to the National Institute on Alcohol Abuse and Alcoholism.) “Alcohol kills many more people than many may realize,” said Yusuf Ransome, an assistant professor at Yale’s School of Public Health. “It is a major contributor to deaths linked to physical injuries, interpersonal violence, motor vehicle crashes, self-harm and other harmful outcomes.” One reason for this might be that alcohol is often viewed as socially acceptable. “Alcohol use has been normalized because it is consumed sometimes at family and communal gatherings, casual outings, and that’s the type of drinking that is typically seen or showed within the media,” he said. “We rarely see the long-term health impacts of excessive alcohol use, nor do we show the acute dangers of alcohol misuse and abuse.” Between 2000 and 2016, according to research published in JAMA, alcohol-related deaths continually increased for white men (2.3 percent per year on average) and white women (4.1 percent), with middle-aged white Americans accounting for the highest increase in deaths. Rapid increases during this period in mortality related to alcohol and drugs like opioids among white Americans — particularly those without a college degree — have been termed “deaths of despair.” Sign up for The Upshot Newsletter: Analysis that explains politics, policy and everyday life, with an emphasis on data and charts. © 2021 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 27779 - Posted: 04.21.2021

Jordana Cepelewicz During every waking moment, we humans and other animals have to balance on the edge of our awareness of past and present. We must absorb new sensory information about the world around us while holding on to short-term memories of earlier observations or events. Our ability to make sense of our surroundings, to learn, to act and to think all depend on constant, nimble interactions between perception and memory. But to accomplish this, the brain has to keep the two distinct; otherwise, incoming data streams could interfere with representations of previous stimuli and cause us to overwrite or misinterpret important contextual information. Compounding that challenge, a body of research hints that the brain does not neatly partition short-term memory function exclusively into higher cognitive areas like the prefrontal cortex. Instead, the sensory regions and other lower cortical centers that detect and represent experiences may also encode and store memories of them. And yet those memories can’t be allowed to intrude on our perception of the present, or to be randomly rewritten by new experiences. A paper published recently in Nature Neuroscience may finally explain how the brain’s protective buffer works. A pair of researchers showed that, to represent current and past stimuli simultaneously without mutual interference, the brain essentially “rotates” sensory information to encode it as a memory. The two orthogonal representations can then draw from overlapping neural activity without intruding on each other. The details of this mechanism may help to resolve several long-standing debates about memory processing. To figure out how the brain prevents new information and short-term memories from blurring together, Timothy Buschman, a neuroscientist at Princeton University, and Alexandra Libby, a graduate student in his lab, decided to focus on auditory perception in mice. They had the animals passively listen to sequences of four chords over and over again, in what Buschman dubbed “the worst concert ever.” All Rights Reserved © 2021

Keyword: Learning & Memory
Link ID: 27778 - Posted: 04.17.2021