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Heidi Ledford Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples1. The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19. The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.” Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper2, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects. She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects. The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28584 - Posted: 12.06.2022

ByErik Stokstad Toxoplasma gondii is sometimes called the “mind control” parasite: It can infect the brains of animals and mess with their behavior in ways that may kill the host but help ensure the parasite’s spread. But now, researchers have found that infected wolves may actually benefit from those mind-altering tricks. A Toxoplasma infection, they found, makes wolves bolder and more likely to become pack leaders or disperse into other habitats, giving them more opportunity to reproduce. "We’ve really underestimated some of the consequences this parasite has,” says Eben Gering, a biologist at Nova Southeastern University who was not involved in the work. “The findings probably represent the tip of the iceberg concerning the parasite’s significance to the dynamics of wild ecosystems.” T. gondii, a single-celled parasite, only reproduces in domesticated cats and other felids. Infected cats excrete spore-packed oocysts in their feces, which can survive on plants or in soil or water. They can also persist in undercooked meat of livestock or game. When a host—humans included—consumes an oocyst, the spores are released and spread into the brain and muscles, forming new cysts. Worldwide, about one in four people is infected. Usually, the immune system keeps the parasite in check, but it can cause spontaneous abortion and other serious problems during pregnancy. It's long been known that rodents infected with Toxoplasma lose their fear of predators. Cysts in the brain somehow increase dopamine and testosterone, boosting boldness and risk-taking and increasing the chance the host will be eaten by cats. "These parasites are using some generic mind control or personality control that helps them fulfill their lifecycle," says Jaap de Roode, a biologist at Emory University who was not involved in the new study. "And that has all sorts of interesting consequences that we may not even have thought of before.” The consequences aren’t limited to rodents. In 2016, researchers in Gabon found that Toxoplasma-infected captive chimpanzees lost their aversion to leopard urine. And last year, another team described how Toxoplasma-infected hyena cubs in Kenya venture closer to lions, making them more likely to be killed.

Keyword: Aggression; Emotions
Link ID: 28583 - Posted: 12.06.2022

By Bruce Bower An ancient hominid dubbed Homo naledi may have lit controlled fires in the pitch-dark chambers of an underground cave system, new discoveries hint. Researchers have found remnants of small fireplaces and sooty wall and ceiling smudges in passages and chambers throughout South Africa’s Rising Star cave complex, paleoanthropologist Lee Berger announced in a December 1 lecture hosted by the Carnegie Institution of Science in Washington, D.C. “Signs of fire use are everywhere in this cave system,” said Berger, of the University of the Witwatersrand, Johannesburg. H. naledi presumably lit the blazes in the caves since remains of no other hominids have turned up there, the team says. But the researchers have yet to date the age of the fire remains. And researchers outside Berger’s group have yet to evaluate the new finds. H. naledi fossils date to between 335,000 and 236,000 years ago (SN: 5/9/17), around the time Homo sapiens originated (SN: 6/7/17). Many researchers suspect that regular use of fire by hominids for light, warmth and cooking began roughly 400,000 years ago (SN: 4/2/12). Such behavior has not been attributed to H. naledi before, largely because of its small brain. But it’s now clear that a brain roughly one-third the size of human brains today still enabled H. naledi to achieve control of fire, Berger contends. Last August, Berger climbed down a narrow shaft and examined two underground chambers where H. naledi fossils had been found. He noticed stalactites and thin rock sheets that had partly grown over older ceiling surfaces. Those surfaces displayed blackened, burned areas and were also dotted by what appeared to be soot particles, Berger said. © Society for Science & the Public 2000–2022.

Keyword: Evolution
Link ID: 28582 - Posted: 12.06.2022

By Roni Caryn Rabin Deaths due to substance abuse, particularly of alcohol and opioids, rose sharply among older Americans in 2020, the first year of the coronavirus pandemic, as lockdowns disrupted routines and isolation and fear spread, federal health researchers reported on Wednesday. Alcohol and opioid deaths remained far less common among older people than among those middled-aged and younger, and rates had been rising in all groups for years. But the pronounced uptick — another data point in the long list of pandemic miseries — surprised government researchers. Deaths from opioids increased among Americans aged 65 and older by 53 percent in 2020 over the previous year, the National Center for Health Statistics found. Alcohol-related deaths, which had already been rising for a decade in this age group, rose by 18 percent. “The rate of alcohol deaths in older people is much lower than for younger adults, but the change caught our eye,” said Ellen Kramarow, a health statistician at the center and the lead author of the report, which analyzed death certificate data. Overdose deaths from synthetic opioids account for fewer than 1 percent of deaths in people over 65, Dr. Kramarow noted. “But the shape of the curve jumped out at us,” she said. Physiological changes that occur with aging leave older adults more vulnerable to the ill effects of alcohol and drugs, as metabolism and excretion of substances slow down, increasing the risk of toxicity. Smaller amounts have bigger effects, researchers have found. Alcohol and opioids can interact poorly with prescription medications that many older adults take for common conditions like hypertension, diabetes and mood disorders. Misuse can lead to falls and injuries, exacerbate underlying medical conditions and worsen declines in cognition. © 2022 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 28581 - Posted: 12.06.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28580 - Posted: 12.03.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28579 - Posted: 12.03.2022

Nicola Davis Science correspondent The brains of teenagers who lived through Covid lockdowns show signs of premature ageing, research suggests. The researchers compared MRI scans of 81 teens in the US taken before the pandemic, between November 2016 and November 2019, with those of 82 teens collected between October 2020 and March 2022, during the pandemic but after lockdowns were lifted. After matching 64 participants in each group for factors including age and sex, the team found that physical changes in the brain that occurred during adolescence – such as thinning of the cortex and growth of the hippocampus and the amygdala – were greater in the post-lockdown group than in the pre-pandemic group, suggesting such processes had sped up. In other words, their brains had aged faster. “Brain age difference was about three years – we hadn’t expected that large an increase given that the lockdown was less than a year [long],” said Ian Gotlib, a professor of psychology at Stanford University and first author of the study. Writing in the journal Biological Psychiatry: Global Open Science, the team report that the participants – a representative sample of adolescents in the Bay Area in California – originally agreed to take part in a study looking at the impact of early life stress on mental health across puberty. As a result, participants were also assessed for symptoms of depression and anxiety. The post-lockdown group self-reported greater mental health difficulties, including more severe symptoms of anxiety, depression and internalising problems. © 2022 Guardian News & Media

Keyword: Stress; Development of the Brain
Link ID: 28578 - Posted: 12.03.2022

Max Barnhart In 2004, when physician Dr. Wilfried Mutombo began treating patients diagnosed with sleeping sickness, the available treatments were themselves horrific and sometimes deadly. "The widely available treatment then was an arsenic-based drug, and it was toxic. It could kill up to 5% of patients," he says. "I lost two of my patients. They were young, and that was a very bad experience. Sleeping sickness is an often fatal disease caused by a parasite where infected people become prone to sleeping all day and night as the disease progresses. It's endemic to 36 countries in Africa, but most cases occur in the Democratic Republic of the Congo. Now, a new oral drug has emerged that is 95% effective at curing sleeping sickness with just one dose. The results of clinical trials for this new drug, acoziborole, were published in The Lancet Infectious Diseases on Nov. 29. It has the potential to drastically change the way sleeping sickness is treated and help the World Health Organization (WHO) reach its goal of eliminating sleeping sickness by 2030. There are two kinds of sleeping sicknesses, both caused by Trypanosoma parasites. The most common form of the disease, and the one treated by this new drug, is caused by Trypanosoma brucei gambiense. Humans are the primary reservoir for the parasite, and it is spread to others by tsetse flies. WHO estimates there were roughly 300,000 cases per year in the late '90s, but the number of cases has now dropped to fewer than 1,000 cases per year. © 2022 npr

Keyword: Sleep
Link ID: 28577 - Posted: 12.03.2022

Darby Saxbe The time fathers devote to child care every week has tripled over the past 50 years in the United States. The increase in fathers’ involvement in child rearing is even steeper in countries that have expanded paid paternity leave or created incentives for fathers to take leave, such as Germany, Spain, Sweden and Iceland. And a growing body of research finds that children with engaged fathers do better on a range of outcomes, including physical health and cognitive performance. Despite dads’ rising participation in child care and their importance in the lives of their kids, there is surprisingly little research about how fatherhood affects men. Even fewer studies focus on the brain and biological changes that might support fathering. It is no surprise that the transition to parenthood can be transformative for anyone with a new baby. For women who become biological mothers, pregnancy-related hormonal changes help to explain why a new mother’s brain might change. But does fatherhood reshape the brains and bodies of men – who don’t experience pregnancy directly – in ways that motivate their parenting? We set out to investigate this question in our recent study of first-time fathers in two countries. Recent research has found compelling evidence that pregnancy can enhance neuroplasticity, or remodeling, in the structures of a woman’s brain. Using magnetic resonance imaging, researchers have identified large-scale changes in the anatomy of women’s brains from before to after pregnancy. In one study, researchers in Spain scanned first-time mothers before conceiving, and again at two months after they gave birth. Compared with childless women, the new mothers’ brain volume was smaller, suggesting that key brain structures actually shrank in size across pregnancy and the early postpartum period. The brain changes were so pronounced that an algorithm could easily differentiate the brain of a woman who had gone through a pregnancy from that of a woman with no children. Copyright © 2010–2022, The Conversation US, Inc.

Keyword: Sexual Behavior; Brain imaging
Link ID: 28576 - Posted: 12.03.2022

By Gina Kolata In a bold attempt to stop the progress of some cases of Alzheimer’s disease, a group of researchers is trying something new — injecting a protective gene into patients’ brains. The trial involved just five patients with a particular genetic risk for Alzheimer’s. They received a very low dose of the gene therapy — a test of safety, which the treatment passed. But the preliminary results, announced Friday during the Clinical Trials on Alzheimer’s Disease conference, showed that proteins from the added gene appeared in the patients’ spinal fluid, and levels in the brain of two markers of Alzheimer’s disease, tau and amyloid, fell. Those findings were promising enough to advance the clinical trial into its next phase. Treatment of another five patients at a higher dose is underway, and the work, initially funded by the nonprofit Alzheimer’s Drug Discovery Foundation, is supported by Lexeo Therapeutics, a fledgling company founded by Dr. Ronald Crystal, who is also chairman of the department of genetic medicine at Weill Cornell Medicine in New York. The hope is to get a stronger response, eventually leading to a treatment that might slow the disease in whom it has started or, even better, protect people at high risk who have no symptoms. “It’s a very provocative, very intriguing approach,” said Dr. Eliezer Masliah, director of the neuroscience division at the National Institute on Aging. Participants in the study are among the approximately 2 percent of people who have inherited a pair of copies of a gene, APOE4, which markedly increases their risk of Alzheimer’s. For the study subjects, the first symptoms of Alzheimer’s had already emerged — their genetic risk had played out, and they had few options. There is no treatment that is directed specifically at APOE4-driven Alzheimer’s, nor is one on the near horizon. © 2022 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 28575 - Posted: 12.03.2022

By Meredith Wadman It just got easier for U.S. scientists to get their hands on some pot—for research, that is. President Joe Biden today signed into law a bill that streamlines access to marijuana for medical research. The new law is expected to speed the issuance of government permits to scientists who want to study cannabis, whose medicinal promise has been widely touted but remains, with a few exceptions, unproven. It will also expedite applications from producers—including universities—that want to grow and distribute the drug for research. It also obliges the federal government to make sure an adequate, uninterrupted supply of marijuana is available to scientists. “We will now be able to treat marijuana like we treat any other substance or pharmaceutical for which we hope there is potential benefit. We will be able to subject it to rigorous scientific trial,” says Representative Andy Harris (R–MD), a physician and former National Institutes of Health (NIH)–funded researcher who helped usher the bipartisan legislation through Congress. “This is exciting,” says Ziva Cooper, the director of the Center for Cannabis and Cannabinoids at the University of California (UC), Los Angeles. “The bill is a significant step forward with respect to chipping away at the barriers” for research. Scientists are eager to study cannabis and its derivatives as potential treatments for cancer, chronic pain, post-traumatic stress disorder, and other conditions. Other cannabis researchers welcomed the new law but said it doesn’t go far enough. In particular, they are disappointed it does not include a provision from an earlier draft of the legislation that would have allowed scientists to buy and study the marijuana available to consumers in the 37 states that have legalized its recreational or medical use.

Keyword: Drug Abuse
Link ID: 28574 - Posted: 12.03.2022

By Kevin Hartnett A mouse is running on a treadmill embedded in a virtual reality corridor. In its mind’s eye, it sees itself scurrying down a tunnel with a distinctive pattern of lights ahead. Through training, the mouse has learned that if it stops at the lights and holds that position for 1.5 seconds, it will receive a reward — a small drink of water. Then it can rush to another set of lights to receive another reward. This setup is the basis for research published in July in Cell Reports by the neuroscientists Elie Adam, Taylor Johns and Mriganka Sur of the Massachusetts Institute of Technology. It explores a simple question: How does the brain — in mice, humans and other mammals — work quickly enough to stop us on a dime? The new work reveals that the brain is not wired to transmit a sharp “stop” command in the most direct or intuitive way. Instead, it employs a more complicated signaling system based on principles of calculus. This arrangement may sound overly complicated, but it’s a surprisingly clever way to control behaviors that need to be more precise than the commands from the brain can be. Control over the simple mechanics of walking or running is fairly easy to describe: The mesencephalic locomotor region (MLR) of the brain sends signals to neurons in the spinal cord, which send inhibitory or excitatory impulses to motor neurons governing muscles in the leg: Stop. Go. Stop. Go. Each signal is a spike of electrical activity generated by the sets of neurons firing. The story gets more complex, however, when goals are introduced, such as when a tennis player wants to run to an exact spot on the court or a thirsty mouse eyes a refreshing prize in the distance. Biologists have understood for a long time that goals take shape in the brain’s cerebral cortex. How does the brain translate a goal (stop running there so you get a reward) into a precisely timed signal that tells the MLR to hit the brakes? Simons Foundation, All Rights Reserved © 2022

Keyword: Movement Disorders
Link ID: 28573 - Posted: 11.30.2022

By Pam Belluck The hotly anticipated results of a clinical trial of an experimental Alzheimer’s drug suggest that the treatment slowed cognitive decline somewhat for people in the early stages of the disease but also caused some patients to experience brain swelling or brain bleeding. The new data, released Tuesday evening, offered the first detailed look at the effects of the drug, lecanemab, and comes two months after its manufacturers, Eisai and Biogen, stoked excitement by announcing that the drug had shown positive results. Alzheimer’s experts said the new information showed reason for both optimism and caution. “The benefit is real; so too are the risks,” said Dr. Jason Karlawish, a co-director of the University of Pennsylvania’s Penn Memory Center, who was not involved in the research. A report of the findings published in the New England Journal of Medicine said that over 18 months, lecanemab “resulted in moderately less decline on measures of cognition and function,” compared with patients receiving a placebo. Still, the study of nearly 1,800 patients with mild symptoms, which was funded by the companies and co-written by scientists at Eisai, concluded that “longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease.” The companies’ initial announcement in September had sent their stock prices soaring because the field of Alzheimer’s drug development has been marked by years of failures. © 2022 The New York Times Company

Keyword: Alzheimers
Link ID: 28572 - Posted: 11.30.2022

Cephalopods like octopuses, squids and cuttlefish are highly intelligent animals with complex nervous systems. In “Science Advances”, a team led by Nikolaus Rajewsky of the Max Delbrück Center has now shown that their evolution is linked to a dramatic expansion of their microRNA repertoire. If we go far enough back in evolutionary history, we encounter the last known common ancestor of humans and cephalopods: a primitive wormlike animal with minimal intelligence and simple eyespots. Later, the animal kingdom can be divided into two groups of organisms – those with backbones and those without. While vertebrates, particularly primates and other mammals, went on to develop large and complex brains with diverse cognitive abilities, invertebrates did not. With one exception: the cephalopods. Scientists have long wondered why such a complex nervous system was only able to develop in these mollusks. Now, an international team led by researchers from the Max Delbrück Center and Dartmouth College in the United States has put forth a possible reason. In a paper published in “Science Advances”, they explain that octopuses possess a massively expanded repertoire of microRNAs (miRNAs) in their neural tissue – reflecting similar developments that occurred in vertebrates. “So, this is what connects us to the octopus!” says Professor Nikolaus Rajewsky, Scientific Director of the Berlin Institute for Medical Systems Biology of the Max Delbrück Center (MDC-BIMSB), head of the Systems Biology of Gene Regulatory Elements Lab, and the paper’s last author. He explains that this finding probably means miRNAs play a fundamental role in the development of complex brains.

Keyword: Evolution; Epigenetics
Link ID: 28571 - Posted: 11.30.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Gary Stix  Many people with bipolar disorder have a strong attraction to marijuana. A 2019 review of 53 studies found that almost a quarter of a combined sample of 51,756 individuals with the condition used cannabis or had a problematic pattern of consumption (cannabis use disorder), compared with 2 to 7 percent in the general population—and an earlier study placed usage estimates still higher. Cannabis and bipolar disorder do not go particularly well together. Consumption may increase manic and psychotic symptoms, and there may be a greater risk of suicide. But can the allure of cannabis be explained as a mere form of substance misuse? Why are people with bipolar disorder so attracted to marijuana? Could they be getting any possible benefit from it? Alannah Miranda of the University of California, San Diego, is a postdoctoral scholar working with U.C.S.D. psychiatry professors William Perry and Arpi Minassian to explore these questions. Miranda presented her and her colleagues’ unpublished work at this year’s giant Society for Neuroscience conference, which attracted more than 24,000 people earlier this month. She talked to Scientific American about what she discovered in this continuing study, which has been funded by the National Institute on Drug Abuse. [An edited transcript of the interview follows.] Tell me about what you’re studying. I’m researching the effects of cannabis on cognition in people with bipolar disorder. People with bipolar disorder report that it’s helping alleviate some of their symptoms in terms of issues related to memory, attention, focus and anxiety. © 2022 Scientific American,

Keyword: Schizophrenia; Drug Abuse
Link ID: 28569 - Posted: 11.30.2022

By Lisa Mulcahy If you’ve ever had your vision “white out” (or “gray out”), you’ve probably felt a little unnerved by the experience. “You’ll see a bright light, and your vision will go pale,” says Teri K. Geist, an optometrist and trustee of the American Optometry Association. As disconcerting as they are, vision whiteouts are usually benign. Making sure, though, means talking with a physician or optometrist. Before you do, here are some things to consider. If you have recurrent whiteouts, counting their duration in real time can help get you the correct diagnosis. Note any specific details the whiteouts appear to have in common. Do they happen right after you stand up from a chair, for example? Most often, whiteouts occur when a person is ready to pass out because of a sudden drop in blood pressure. About 1 in 3 people will faint at some point in their lives. “Fainting can be benign when it’s related to a sudden stress,” says Sarah Thornton, a neuro-ophthalmologist at Wills Eye Hospital in Philadelphia. “Standing up too fast, overexerting, becoming dehydrated or taking certain medications can also lead to hypotension — low blood pressure — and potentially, a whiteout.” A less common risk: “Whiteouts can occur with changes in G force,” says Geist, for instance, in a car accident or on a roller coaster. A whiteout caused by physical stress or exertion will clear within just a few minutes. Although fainting is usually benign, always tell your doctor if you’ve fainted — occasionally, whiteouts and fainting are tied to something serious. “An underlying heart condition, such as aortic stenosis, could cause fainting symptoms, including whiteout,” says Dean M. Cestari, a neuro-ophthalmologist at Mass General Brigham Mass Eye and Ear in Boston and associate professor of ophthalmology at Harvard Medical School. Other such conditions can include arrhythmias, heart failure and atrial fibrillation.

Keyword: Vision
Link ID: 28568 - Posted: 11.30.2022

By Sandra G. Boodman The first time it happened, Erin Bousquet was a high school freshman who had been diagnosed with strep throat, a common infection in her family. After three days on an antibiotic, she wasn’t getting better, so the 14-year-old was prescribed a second drug. A day or two later, Kristen Bousquet noticed worrisome changes in her oldest child. Erin seemed “lethargic and out of it,” her mother recalled. She was irritable, her pupils looked dilated, and much of what she said made no sense. Most alarming was Erin’s newfound ability to sleep for up to 20 hours at a time. “It was quite scary,” Kristen recalled. “At first we thought she was joking.” That bizarre episode, which occurred in September 2017, has been followed by 11 more, each lasting an average of 10 days. Between episodes, Erin’s behavior is normal. For 2 1/2 years she and her parents, who live in Lincoln, Neb., consulted pediatric neurologists, a neurosurgeon, an obstetrician-gynecologist and other specialists in a largely fruitless search to identify the condition that drastically alters her personality and temporarily shuts down her life two or three times a year. The diagnosis, made in March 2020, was an enormous relief. But it has required the Bousquets to cope with continued uncertainty because so little is known about Erin’s disorder. “The hardest thing for me are the things I’ve missed out on,” said Erin, a 19-year-old sophomore at the University of Nebraska at Lincoln. They include a high school basketball championship, her 18th birthday, a family Christmas trip to Colorado and the start of her sophomore year of college. Erin slept through them all. Because her symptoms — disorientation and prolonged sleep — can be signs of a serious, even life-threatening, illness, the staff at the urgent care clinic where Erin had been treated for strep told her mother to take her to an emergency room. A test for infectious mononucleosis, a contagious virus common among adolescents and young adults that causes profound fatigue was negative and a quick neurological exam was normal. Erin was sent home.

Keyword: Sleep
Link ID: 28567 - Posted: 11.23.2022

By Ingrid Wickelgren  Science has largely neglected pregnancy’s effect on the brain, even though it involves dramatic surges in steroid hormones, which are known to alter the organ. A decade ago neuroscientist Elseline Hoekzema, then a young postdoctoral fellow thinking about having her first child, and two of her female colleagues set out to bridge the knowledge gap. “There’s this enormous event involving such strong hormone changes,” says Hoekzema, now at Amsterdam University Medical Center. “It’s really weird that so little was known about this.” Their initial study, published in 2016, revealed for the first time that pregnancy produced significant structural changes in a woman’s brain that endured for at least two years after birth. Now in a new seven-year study, Hoekzema and her colleagues have seen the same structural changes in different women and have shown that pregnancy also alters the function of a key brain network involved in self-reflection. According to the work, which appeared on Nov. 22 in Nature Communications, the brain changes correlate with a mother’s enhanced bonding with her baby. The findings were derived from examining the female participants’ physiology and using questionnaires to assess their behavior and mental state. And for the first time in humans, the researchers found strong evidence that female hormones are behind it all. The biggest changes occur in a brain network that is active when the brain is idling—that is, when it is not engaged in any particular task—suggesting that pregnancy alters the organ’s baseline state. “[The researchers] are seeing these functional connectivity changes even at rest,” says Jodi Pawluski, a neuroscientist at the University of Rennes 1 in France, who studies the maternal brain and perinatal mental illness but was not involved in the study. “That speaks to the significance of this stage in a birthing person’s life and how it really is transformative in the brain.”

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 28566 - Posted: 11.23.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022