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By Rachel Nuwer In an important step toward medical approval, MDMA, the illegal drug popularly known as Ecstasy or Molly, was shown to bring relief to those suffering from severe post-traumatic stress disorder when paired with talk therapy. Of the 90 people who took part in the new study, which is expected to be published later this month in Nature Medicine, those who received MDMA during therapy experienced a significantly greater reduction in the severity of their symptoms compared with those who received therapy and an inactive placebo. Two months after treatment, 67 percent of participants in the MDMA group no longer qualified for a diagnosis of PTSD, compared with 32 percent in the placebo group. MDMA produced no serious adverse side effects. Some participants temporarily experienced mild symptoms like nausea and loss of appetite. “This is about as excited as I can get about a clinical trial,” said Gul Dolen, a neuroscientist at Johns Hopkins University School of Medicine, who was not involved in the research. “There is nothing like this in clinical trial results for a neuropsychiatric disease.” Before MDMA-assisted therapy can be approved for therapeutic use, the Food and Drug Administration needs a second positive Phase 3 trial, which is currently underway with 100 participants. Approval could come as early as 2023. Mental health experts say that this research — the first Phase 3 trial conducted on psychedelic-assisted therapy — could pave the way for further studies on MDMA’s potential to help address other difficult-to-treat mental health conditions, including substance abuse, obsessive compulsive disorder, phobias, eating disorders, depression, end-of-life anxiety and social anxiety in autistic adults. © 2021 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 27804 - Posted: 05.05.2021

By Nicholas Bakalar Type 2 diabetes is a chronic, progressive illness that can have devastating complications, including hearing loss, blindness, heart disease, stroke, kidney failure and vascular damage so severe as to require limb amputation. Now a new study underscores the toll that diabetes may take on the brain. It found that Type 2 diabetes is linked to an increased risk for Alzheimer’s disease and other forms of dementia later in life, and the younger the age at which diabetes is diagnosed, the greater the risk. The findings are especially concerning given the prevalence of diabetes among American adults and rising rates of diabetes in younger people. Once referred to as “adult-onset diabetes” to distinguish it from the immune-related “juvenile-onset” Type 1 disease that begins in childhood, Type 2 diabetes is seen in younger and younger people, largely tied to rising rates of obesity. The Centers for Disease Control and Prevention estimates that more than 34 million American adults have Type 2 diabetes, including more than a quarter of those 65 and over. About 17.5 percent of those aged 45 to 64 have Type 2 disease, as do 4 percent of 18- to 44-year-olds. “This is an important study from a public health perspective,” said the director of the Yale Diabetes Center, Dr. Silvio Inzucchi, who was not involved in the research. “The complications of diabetes are numerous, but the brain effects are not well studied. Type 2 diabetes is now being diagnosed in children, and at the same time there’s an aging population.” © 2021 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 27803 - Posted: 05.05.2021

By Jane E. Brody Look and you shall see: A generation of the real-life nearsighted Mr. Magoos is growing up before your eyes. A largely unrecognized epidemic of nearsightedness, or myopia, is afflicting the eyes of children. People with myopia can see close-up objects clearly, like the words on a page. But their distance vision is blurry, and correction with glasses or contact lenses is likely to be needed for activities like seeing the blackboard clearly, cycling, driving or recognizing faces down the block. The growing incidence of myopia is related to changes in children’s behavior, especially how little time they spend outdoors, often staring at screens indoors instead of enjoying activities illuminated by daylight. Gone are the days when most children played outside between the end of the school day and suppertime. And the devastating pandemic of the past year may be making matters worse. Susceptibility to myopia is determined by genetics and environment. Children with one or both nearsighted parents are more likely to become myopic. However, while genes take many centuries to change, the prevalence of myopia in the United States increased from 25 percent in the early 1970s to nearly 42 percent just three decades later. And the rise in myopia is not limited to highly developed countries. The World Health Organization estimates that half the world’s population may be myopic by 2050. Given that genes don’t change that quickly, environmental factors, especially children’s decreased exposure to outdoor light, are the likely cause of this rise in myopia, experts believe. Consider, for example, factors that keep modern children indoors: an emphasis on academic studies and their accompanying homework, the irresistible attraction of electronic devices and safety concerns that demand adult supervision during outdoor play. All of these things drastically limit the time youngsters now spend outside in daylight, to the likely detriment of the clarity of their distance vision. © 2021 The New York Times Company

Keyword: Vision; Development of the Brain
Link ID: 27802 - Posted: 05.05.2021

by Peter Hess Deleting the autism-related gene CHD8 from the intestines induces significant gastrointestinal and behavioral changes in mice, according to a new unpublished study. The results suggest that changes to the gut are involved in some of the behavioral traits seen in people with CHD8 mutations, says lead researcher Evan Elliott, assistant professor of molecular and behavioral neuroscience at Bar-Ilan University in Ramat Gan, Israel. Elliott’s team presented the findings virtually this week at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Up to 90 percent of people with CHD8 mutations report gastrointestinal issues such as constipation, Elliott says. Most also have autism. Mice missing one copy of CHD8 have unusually thin and permeable small intestines, Elliott and his colleagues found. The reason seems to be that these mice have fewer mucus-producing goblet cells than controls, resulting in thinner organ walls and less mucus lining the digestive tract. CHD8 regulates the expression of other genes, so Elliott’s team looked at gene expression levels in the CHD8 mice’s intestinal epithelial cells via RNA sequencing. The mice expressed 920 genes differently than control mice did. These include an increase in the expression of genes involved in inflammatory responses and in antimicrobial activity. The latter set may be the body’s way of compensating for increased microbial populations, Elliott says. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27801 - Posted: 05.05.2021

Researchers are now able to wirelessly record the directly measured brain activity of patients living with Parkinson’s disease and to then use that information to adjust the stimulation delivered by an implanted device. Direct recording of deep and surface brain activity offers a unique look into the underlying causes of many brain disorders; however, technological challenges up to this point have limited direct human brain recordings to relatively short periods of time in controlled clinical settings. This project, published in the journal Nature Biotechnology, was funded by the National Institutes of Health’s Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative. “This is really the first example of wirelessly recording deep and surface human brain activity for an extended period of time in the participants’ home environment,” said Kari Ashmont, Ph.D., project manager for the NIH BRAIN Initiative. “It is also the first demonstration of adaptive deep brain stimulation at home.” Deep brain stimulation (DBS) devices are approved by the U. S. Food and Drug Administration for the management of Parkinson’s disease symptoms by implanting a thin wire, or electrode, that sends electrical signals into the brain. In 2018, the laboratory of Philip Starr, M.D., Ph.D. at the University of California, San Francisco, developed an adaptive version of DBS that adapts its stimulation only when needed based on recorded brain activity. In this study, Dr. Starr and his colleagues made several additional improvements to the implanted technology.

Keyword: Brain imaging
Link ID: 27800 - Posted: 05.05.2021

Elena Renken A hundred years ago, the Japanese scientist Y. Shirai published a mysterious finding: When Shirai transplanted tumor tissue into a mouse’s body, the tissue was destroyed by its immune system. But when tumors were grafted in various places in the mouse’s brain, they grew. Tumors seemed to be able to safely hide in the brain, escaping the immune system’s notice. Similar results soon piled up, and scientific consensus accepted the brain as having “immune privilege” — a kind of separation from the immune system. This notion made some sense. Immune cells, in the course of fighting infections, can damage or destroy healthy tissue. Protecting neurons from this damage is more crucial than protecting cells like those in the liver or skin, because neurons typically can’t regenerate. “If they die, they die,” said Justin Rustenhoven, an immunologist at Washington University in St. Louis. “We have a very poor ability to replace them.” In the last couple of decades, though, the idea of immune privilege has withered in the face of mounting evidence that the brain and the immune system do interact. Researchers have tracked immune cells crossing from the bloodstream into the nervous system in animals with brain disease, for instance, and they’ve observed cognitive deficits in mice that lack certain immune cells. Now, Rustenhoven and collaborators have identified how evolution achieves a balancing act, limiting the dangers of immune responses in the central nervous system while still providing protection from disease. The researchers reported recently in the journal Cell that the immune system operates from a distance to constantly inspect the brain for signs of trouble. Immune cells, rather than making themselves at home throughout the brain itself, patrol the sidelines until they detect a threat. All Rights Reserved © 2021

Keyword: Neuroimmunology
Link ID: 27799 - Posted: 05.01.2021

Ariana Remmel Scientists in search of psychedelic drug treatments have developed a way to determine whether a molecule is likely to cause hallucinations, without testing it on people or animals. Growing evidence suggests that psychedelic compounds, which are active in the brain, have potential to treat psychiatric illnesses such as post-traumatic stress disorder (PTSD), but researchers are trying to find out whether there is a way to keep the beneficial properties of these drugs without the hallucinogenic side effects, which can complicate treatment. It is currently almost impossible to predict whether a potential drug will cause hallucinations before it is tested on animals or people. “That really slows down drug discovery,” says David Olson, a chemical neuroscientist at the University of California, Davis. To address this, a team led by Olson and neuroscientist Lin Tian, also at Davis, designed a fluorescent sensor to predict whether a molecule is hallucinogenic, based on the structure of a brain receptor targeted by psychedelics. Using their approach, the researchers identified a psychedelic-like molecule without hallucinogenic properties that they later found had antidepressant activity in mice1. The discovery adds “more fuel for the fire” of efforts to make drugs from psychedelic-like molecules without side effects, says Bryan Roth, a molecular pharmacologist at the University of North Carolina School of Medicine in Chapel Hill. © 2021 Springer Nature Limited

Keyword: Drug Abuse; Stress
Link ID: 27798 - Posted: 05.01.2021

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