By Natalie Angier Julia, her friends and family agreed, had style. When, out of the blue, the 18-year-old chimpanzee began inserting long, stiff blades of grass into one or both ears and then went about her day with her new statement accessories clearly visible to the world, the other chimpanzees at the Chimfunshi wildlife sanctuary in Zambia were dazzled. Pretty soon, they were trying it, too: first her son, then her two closest female friends, then a male friend, out to eight of the 10 chimps in the group, all of them struggling, in front of Julia the Influencer — and hidden video cameras — to get the grass-in-the-ear routine just right. “It was quite funny to see,” said Edwin van Leeuwen of the University of Antwerp, who studies animal culture. “They tried again and again without success. They shivered through their whole bodies.” Dr. van Leeuwen tried it himself and understood why. “It’s not a pleasant feeling, poking a piece of grass far enough into the ear to stay there,” he said. But once the chimpanzees had mastered the technique, they repeated it often, proudly, almost ritualistically, fiddling with the inserted blades to make sure others were suitably impressed. Julia died more than two years ago, yet her grassy-ear routine — a tradition that arose spontaneously, spread through social networks and skirts uncomfortably close to a human meme or fad — lives on among her followers in the sanctuary. The behavior is just one of many surprising examples of animal culture that researchers have lately divulged, as a vivid summary makes clear in a recent issue of Science. Culture was once considered the patented property of human beings: We have the art, science, music and online shopping; animals have the instinct, imprinting and hard-wired responses. But that dismissive attitude toward nonhuman minds turns out to be more deeply misguided with every new finding of animal wit or whimsy: Culture, as many biologists now understand it, is much bigger than we are. © 2021 The New York Times Company

Keyword: Evolution
Link ID: 27809 - Posted: 05.08.2021

by Laura Dattaro Many genes linked to autism, schizophrenia and developmental delay share the same functions: They regulate the expression of other genes and support communication between neurons, according to an unpublished study. Researchers presented the findings virtually today at the 2021 International Society for Autism Research annual meeting. (Links to abstracts may work only for registered conference attendees.) Hundreds of genes with diverse functions are linked to autism, but how each contributes to the condition is unclear. In the new work, researchers analyzed the functions of 102 autism-linked genes that previous studies identified by comparing the genetic sequences of thousands of people with autism and those with other conditions, along with their family members and controls. “The genes identified give us an unprecedented opportunity to follow the biology, follow the genetics, to ask the question, where does this converge on function?” said lead investigator Stephan Sanders while presenting the work. Sanders is associate professor of psychiatry at the University of California, San Francisco. Other researchers are studying convergence in 3D brain models called organoids and looking for neuroanatomical similarities and differences across different animal models of autism, including mice and frogs. “Distinguishing causal functions from non-causal functions of these genes is a massive challenge,” Sanders says, and finding points of convergence could help. “The ultimate goal is to identify why disrupting these genes leads to autism.” © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27808 - Posted: 05.08.2021

Joanne Silberner Scientists once compared the abilities of humans versus canines in tracking a trail of chocolate essential oil laid down in an open field. Though the humans weren't nearly as proficient as the dogs, they did get better with practice. Vladimir Godnik/Getty Images/fStop About 25 years ago, after a particularly bad cold, I suddenly lost my sense of smell — I could no longer sense the difference between sweaty tennis shoes and a fragrant rose. Since then, my olfactory discernment comes and goes, and most of the time it's just gone. I always figured there wasn't much I could do about that, and it hasn't been terrible. My taste buds still work, and I adore fine chocolate. But when COVID-19 hit, the inability to detect odors and fragrances became a diagnostic symptom that upset a lot of COVID-19 sufferers, many of whom also lost their sense of taste. That got me thinking — what does it really mean to have a disordered sense of smell? Does it matter that with my eyes closed I can't tell if I'm in an overripe gym or a perfume store? And is there hope that I'll ever again be able to smell a wet dog or freesia or a gas leak or a raw onion? Scientists explain that when you put your nose in the way of steam rising from a hot cup of coffee, molecules called odorants rise up and land high up in your nose. And when you take a swig of that same joe, as the liquid goes down your throat, some molecules rise upward and hit that sweet spot. Nerve cells there have receptors that recognize specific molecules, and those nerve cells extend directly into the brain. "That's how you tell you're smelling coffee as opposed to pizza," says Pamela Dalton of the Monell Chemical Senses Center in Philadelphia, who studies how we perceive good smells and bad. When the coffee "odorants" connect with their nerve cells, she says, your brain knows that you've just enjoyed your morning brew. © 2021 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27807 - Posted: 05.08.2021

By Paul E. Greenberg Since the early 1990s, I, together with my colleagues, have been studying the economic burden of adults with major depressive disorders (MDD). Over that time, we have tracked shifts in the prevalence of this disease; in the makeup of those suffering from it; and in the nature of treatment both for the disease itself and for the host of comorbidities, such as pain and anxiety disorders, that accompany it. We have then used these data as the basis for calculating the incremental economic burden of adults with MDD—that is, the additional costs traceable to those suffering from the disease in terms of both medical treatment and workplace productivity impacts. Our most recent study was just published in a special issue of PharmacoEconomics (which I also co-edited) that presents new research on the economics of MDD. By focusing on one year during the Great Recession (2010) and another after a long macroeconomic expansion (2018), our analysis provides a helpful profile of the changing economic effects of this widespread and pernicious illness. We report our latest estimates showing that the incremental economic burden of adults with MDD was $326 billion in 2018, 38 percent higher than in 2010. But our work goes deeper than simply providing an economic calculator. This research offers a multifaceted lens through which we can gain a better understanding of how the myriad effects of the illness manifest themselves. Importantly, we find that only 11 percent of the overall burden of illness was attributable to the direct medical costs of treating MDD itself, while the costs of treating comorbid medical conditions made up 24 percent. Another 4 percent was due to suicide-related costs, while fully 61 percent of the total burden in 2018 resulted from a combination of elevated workplace absenteeism and presenteeism (that is, reduced productivity as a result of working while sick). This striking imbalance between medical expenditures to treat either MDD or its comorbidities on the one hand and workplace-related costs on the other is one aspect of the story that has changed dramatically since 2010, when medical costs were equivalent to workplace costs. © 2021 Scientific American,

Keyword: Depression
Link ID: 27806 - Posted: 05.08.2021

By Christina Caron Finding a therapist can be a tough and time-consuming process involving multiple phone calls, waiting lists and insurance hurdles. But what if you were able to walk into your corner drugstore for a bottle of shampoo and also had the option of scheduling a walk-in session for mental health treatment? That’s the future that CVS, the largest retail pharmacy in the United States, is envisioning. Since January the company has added licensed clinical social workers trained in cognitive behavioral therapy to 13 locations in the Houston, Philadelphia and Tampa metro areas. The providers will offer mental health assessments, referrals and counseling either in person or via telehealth, a CVS spokeswoman said, and this spring the company plans to expand to 34 locations in those same regions. The social workers are available during the day, and also on evenings and weekends in the company’s MinuteClinics, which provide a variety of nonemergency health care services either via walk-in or by appointment. The hours are more flexible than what therapists might normally offer, and the social workers partner with the clinic’s nurse practitioners and pharmacists to give prescriptions when needed, said Dr. Daniel Knecht, the vice president of clinical product at CVS Health. CVS is just one of a growing number of retailers who are recognizing the unmet need for mental health providers and hoping to fill the gap. On Thursday, Walmart announced it is acquiring MeMD, which offers online medical and mental health care. Walmart currently provides counseling via Walmart Health, a health center located in a separate building alongside Walmart Supercenters. In Georgia, Walmart Health offers in-person mental health counseling and in Arkansas customers can receive online counseling. Later this year, counseling services will become available at Walmart Health locations in Illinois and Florida, a spokeswoman said. © 2021 The New York Times Company

Keyword: Depression
Link ID: 27805 - Posted: 05.08.2021

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