By Carl Zimmer Edward O. Wilson, a biologist and author who conducted pioneering work on biodiversity, insects and human nature — and won two Pulitzer Prizes along the way — died on Sunday in Burlington, Mass. He was 92. His death was announced on Monday by the E.O. Wilson Biodiversity Foundation. When Dr. Wilson began his career in evolutionary biology in the 1950s, the study of animals and plants seemed to many scientists like a quaint, obsolete hobby. Molecular biologists were getting their first glimpses of DNA, proteins and other invisible foundations of life. Dr. Wilson made it his life’s work to put evolution on an equal footing. “How could our seemingly old-fashioned subjects achieve new intellectual rigor and originality compared to molecular biology?” he recalled in 2009. He answered his own question by pioneering new fields of research. As an expert on insects, Dr. Wilson studied the evolution of behavior, exploring how natural selection and other forces could produce something as extraordinarily complex as an ant colony. He then championed this kind of research as a way of making sense of all behavior — including our own. As part of his campaign, Dr. Wilson wrote a string of books that influenced his fellow scientists while also gaining a broad public audience. “On Human Nature” won the Pulitzer Prize for general nonfiction in 1979; “The Ants,” which Dr. Wilson wrote with his longtime colleague Bert Hölldobler, won him his second Pulitzer, in 1991. © 2021 The New York Times Company

Keyword: Evolution
Link ID: 28125 - Posted: 12.29.2021

By Karen Brown For decades, Linda Larson has been trying to distance herself from the diagnosis she was given as a teenager: schizophrenia. She accepts that she has the mental disorder but deeply resents the term’s stigma. People hear it and think, “violent, amoral, unhygienic,” she said. Ms. Larson, 74, is part of a group trying to remove that association — by changing the name of the illness. The idea is that replacing the term “schizophrenia” with something less frightening and more descriptive will not only change how the public perceives people with the diagnosis, but also how these people see themselves. Ms. Larson is a member of the Consumer Advisory Board of the Massachusetts Mental Health Center, which is associated with Beth Israel Deaconess Medical Center in Boston. The group has been working with psychiatrists at Harvard to build momentum for a name change, most recently through a national survey published in the journal Schizophrenia Research. “That term over time has become so associated with hopelessness, with dangerousness, with volatile and erratic behavior, that doctors are afraid to use that term with people and their family members,” said Dr. Raquelle Mesholam-Gately, a Harvard psychologist and the lead author of the new paper. “And people who have the condition don’t want to be associated with that name.” As a result, she said, clinicians often avoid making such a devastating diagnosis and many patients and their families don’t seek treatment until after the illness has wreaked considerable damage. Dr. Mesholam-Gately and her team asked about 1,200 people connected to schizophrenia — including those with the disorder, their family members, mental health providers, researchers and government officials — whether it should be called something else. The survey proposed nine alternative names, based partly on the experience of people diagnosed with schizophrenia. Among them: altered perception disorder, attunement disorder, disconnectivity syndrome, integration disorder and psychosis spectrum disorder. © 2021 The New York Times Company

Keyword: Schizophrenia
Link ID: 28124 - Posted: 12.22.2021

By Christof Koch A young Ernest Hemingway, badly injured by an exploding shell on a World War I battlefield, wrote in a letter home that “dying is a very simple thing. I’ve looked at death, and really I know. If I should have died it would have been very easy for me. Quite the easiest thing I ever did.” Years later Hemingway adapted his own experience—that of the soul leaving the body, taking flight and then returning—for his famous short story “The Snows of Kilimanjaro,” about an African safari gone disastrously wrong. The protagonist, stricken by gangrene, knows he is dying. Suddenly, his pain vanishes, and Compie, a bush pilot, arrives to rescue him. The two take off and fly together through a storm with rain so thick “it seemed like flying through a waterfall” until the plane emerges into the light: before them, “unbelievably white in the sun, was the square top of Kilimanjaro. And then he knew that there was where he was going.” The description embraces elements of a classic near-death experience: the darkness, the cessation of pain, the emerging into the light and then a feeling of peacefulness. Peace Beyond Understanding Near-death experiences, or NDEs, are triggered during singular life-threatening episodes when the body is injured by blunt trauma, a heart attack, asphyxia, shock, and so on. About one in 10 patients with cardiac arrest in a hospital setting undergoes such an episode. Thousands of survivors of these harrowing touch-and-go situations tell of leaving their damaged bodies behind and encountering a realm beyond everyday existence, unconstrained by the usual boundaries of space and time. These powerful, mystical experiences can lead to permanent transformation of their lives. © 2021 Scientific American,

Keyword: Consciousness; Stress
Link ID: 28123 - Posted: 12.22.2021

by Anna Goshua A variety of traits, including developmental delay and intellectual disability, characterize people with mutations in the autism-linked gene MYT1L, according to a new study. The gene encodes a transcription factor important for cells that make myelin, which insulates nerve cells and is deficient in some forms of autism. The work, published 8 November in Human Genetics, represents the most detailed study of the traits associated with MYT1L mutations to date. “We wanted to gather more cases to bring a clearer clinical and molecular picture of the condition for lab scientists, clinicians and also for patients and families,” says study investigator Juliette Coursimault, a physician-researcher in the genetics department at Rouen University Hospital in France. She and her co-researchers described 62 people, whereas previous literature included only 12 cases. The new characterization will “benefit clinicians’ diagnosis and treatment strategies when a patient with MYT1L mutation arrives in their clinic,” says Brady Maher, a lead investigator at the Lieber Institute for Brain Development at Johns Hopkins University in Baltimore, Maryland, who was not part of the study. The researchers identified and reviewed data for 22 people with MYT1L mutations who had been described in the academic literature, and collected clinical and molecular data from an additional 40 people, aged 1 to 34 years old, with likely or confirmed pathogenic variants of MYT1L. They recruited the participants through Rouen University Hospital and data-sharing networks such as GeneMatcher, which connects clinicians and researchers. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28122 - Posted: 12.22.2021

By Gretchen Reynolds People who work out regularly and are aerobically fit tend to guzzle a surprising amount of alcohol, according to a new study, well timed for the holidays, of the interplay between fitness, exercise and imbibing. The study, which involved more than 40,000 American adults, finds that active, physically fit men and women are more than twice as likely to be moderate or heavy drinkers as people who are out of shape. The results add to mounting evidence from previous studies — and many of our bar tabs — that exercise and alcohol frequently go hand in hand, with implications for the health effects of each. Many people, and some researchers, might be surprised to learn how much physically active people tend to drink. In general, people who take up one healthy habit, such as working out, tend to practice other salubrious habits, a phenomenon known as habit clustering. Fit, active people seldom smoke, for instance, and tend to eat healthful diets. So, it might seem logical that people who often exercise would drink alcohol sparingly. But multiple studies in recent years have found close ties between working out and tippling. In one of the earliest, from 2001, researchers used survey answers from American men and women to conclude that moderate drinkers, defined in that study as people who finished off about a drink a day, were twice as likely as those who didn’t drink at all to exercise regularly. Later studies found similar patterns among college athletes, who drank substantially more than other collegians, a population not famous for its temperance. © 2021 The New York Times Company

Keyword: Drug Abuse; Obesity
Link ID: 28121 - Posted: 12.22.2021

By Cara Giaimo Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. It’s tough out there for a mouse. Outdoors, its enemies lurk on all sides: owls above, snakes below, weasels around the bend. Indoors, a mouse may find itself targeted by broom-wielding humans or bored cats. Mice compensate with sharp senses of sight, hearing and smell. But they may have another set of tools we’ve overlooked. A paper published last week in Royal Society Open Science details striking similarities between the internal structures of certain small mammal and marsupial hairs and those of man-made optical instruments. In this paper as well as other unpublished experiments, the author, Ian Baker, a physicist who works in private industry, posits that these hairs may act as heat-sensing “infrared antennae” — further cluing the animals into the presence of warm-blooded predators. Although much more work is necessary to connect the structure of these hairs to this potential function, the study paints an “intriguing picture,” said Tim Caro, a professor of evolutionary ecology at the University of Bristol in England who was not involved. Dr. Baker has spent decades working with thermal imaging cameras, which visualize infrared radiation produced by heat. For his employer, the British defense company Leonardo UK Ltd., he researches and designs infrared sensors. But in his spare time he often takes the cameras to fields and forests near his home in Southampton, England, to film wildlife. Over the years, he has developed an appreciation for “how comfortable animals are in complete darkness,” he said. That led him to wonder about the extent of their sensory powers. © 2021 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 28120 - Posted: 12.18.2021

Mir Jalil Razavi Weiying Dai The human brain has been called the most complex object in the known universe. And with good reason: It has around 86 billion neurons and several hundred thousand miles of axon fibers connecting them. Unsurprisingly, the process of brain folding that results in the brain’s characteristic bumps and grooves is also highly complex. Despite decades of speculation and research, the underlying mechanism behind this process remains poorly understood. As biomechanics and computer science researchers, we have spent several years studying the mechanics of brain folding and ways to visualize and map the brain, respectively. Figuring out this complexity may help researchers better diagnose and treat developmental brain disorders such as lissencephaly, or smooth brain, and epilepsy. Because many neurological disorders emerge at the early stages of development, understanding how brain folding works can provide useful insights into normal and pathological brain function. The mechanics of brain folding The brain is made of two layers. The outer layer, called the cerebral cortex, is composed of folded gray matter made up of small blood vessels and the spherical cell bodies of billions of neurons. The inner layer is composed of white matter, consisting mostly of the neurons’ elongated tails, called myelinated axons. When a story fascinates you, remember: Your donations make it possible Illustration of cross section of brain showing axonal pathways transitioning from gray matter into white matter. In recent years, researchers have shown that mechanics, or the forces that objects exert on one another, play an important role in the growth and folding of the brain. © 2010–2021, The Conversation US, Inc.

Keyword: Development of the Brain
Link ID: 28119 - Posted: 12.18.2021

Rafael Yuste Michael Levin In the middle of his landmark book On the Origin of Species, Darwin had a crisis of faith. In a bout of honesty, he wrote, “To suppose that the eye with all its inimitable contrivances for adjusting the focus to different distances, for admitting different amounts of light, and for the correction of spherical and chromatic aberration, could have been formed by natural selection, seems, I confess, absurd in the highest degree.” While scientists are still working out the details of how the eye evolved, we are also still stuck on the question of how intelligence emerges in biology. How can a biological system ever generate coherent and goal-oriented behavior from the bottom up when there is no external designer? In fact, intelligence—a purposeful response to available information, often anticipating the future—is not restricted to the minds of some privileged species. It is distributed throughout biology, at many different spatial and temporal scales. There are not just intelligent people, mammals, birds and cephalopods. Intelligent, purposeful problem-solving behavior can be found in parts of all living things: single cells and tissues, individual neurons and networks of neurons, viruses, ribosomes and RNA fragments, down to motor proteins and molecular networks. Arguably, understanding the origin of intelligence is the central problem in biology—one that is still wide open. In this piece, we argue that progress in developmental biology and neuroscience is now providing a promising path to show how the architecture of modular systems underlies evolutionary and organismal intelligence. © 2021 Scientific American

Keyword: Evolution; Development of the Brain
Link ID: 28118 - Posted: 12.18.2021

Jon Hamilton Scientists may have learned why opioids depress breathing while relieving pain. The finding could lead to pain drugs that don't cause respiratory failure, the usual cause of death in opioid overdoses. When people feel pain, they tend to breathe faster. When they take an opioid to kill that pain, their breathing slows down. Now scientists think they know how pain and respiration are connected in the brain. NPR's Jon Hamilton reports that the discovery could eventually lead to safer pain drugs. JON HAMILTON, BYLINE: Sung Han has been studying the link between pain and breathing in his lab at the Salk Institute in San Diego. But he got a real-world demonstration recently while taking a shower. SUNG HAN: I forgot to change the temperature, and the cold water just suddenly came out and covered my entire body. And then I just - I was breathing really fast. HAMILTON: A typical reaction to what Han calls aversive sensory information - and he thinks he knows the cause. Han's lab has identified a brain circuit in mice that appears to link the emotional experience of pain to breathing rhythm. Han says the circuit involves two populations of brain cells both found in the same small area of the brain stem. HAN: One population regulate pain and the other population regulate breathing, and that's the reason why pain and breathing are interacting each other. HAMILTON: They're linked together. If that's also true in people, it would help explain the mysterious connection between breathing and emotion, which has puzzled scientists for centuries. And the finding, which appears in the journal Neuron, could also have practical applications. That's because both groups of brain cells - the ones for breathing and the ones for pain - respond to opioids. Han says this is why an overdose can be fatal. © 2021 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 28117 - Posted: 12.18.2021

By Richard Sandomir Allan Rechtschaffen, an indefatigable sleep researcher at the University of Chicago who tested the effects of sleep deprivation, studied dreaming, narcolepsy, napping and insomnia and standardized the measurement of sleep stages, died on Nov. 29 at his home in Chicago. He was 93. His wife, Karen Rechtschaffen, confirmed the death. The University of Chicago was an established center of sleep research when Professor Rechtschaffen arrived on its campus in 1957 as a psychology instructor. Four years earlier, Nathaniel Kleitman, a physiologist, and Eugene Aserinsky, a graduate student, had written a paper that reported the discovery of rapid eye movement, or REM, during sleep, an indication of dreaming. The finding appealed to Professor Rechtschaffen’s fascination with the mind’s effect on the body. “This was a perfect vehicle for studying that issue,” he said in an interview in 2010 with the Sleep Research Society, which he helped start 50 years earlier. “You could conceive of it as the mind turning on with the REM period and turning off with the end of the REM period. So you could see periods of mind and periods of no mind.” REM and other aspects of sleep became the focus of his career. In 1958, he was named director of the university’s sleep research laboratory, where his experiments on animals and humans over the next 41 years helped him define a challenge that he described this way: “If sleep doesn’t serve an absolutely vital function, it is the biggest mistake evolution ever made.” His best-known experiment concerned self-deprivation using rats. As Professor Rechtschaffen and his colleagues reported in the journal Science in 1983, they had placed two rats at a time in a plexiglass box, each with an electrode attached from its head to a computer and each placed on one-half of a divided disk built over shallow water. When the experimental rat tried to sleep, the disk automatically rotated, forcing the animal to stay awake. The control rat was treated similarly but could sleep when the other rat was awake and the disk was not moving. © 2021 The New York Times Company

Keyword: Sleep
Link ID: 28116 - Posted: 12.18.2021

by Anna Goshua Researchers have identified hundreds of genes that may contribute to autism, but these genes can’t fully account for the condition’s traits. Studies from the past decade implicate an additional layer of ‘epigenetic’ complexity: chemical tags called methyl groups laid on top of a person’s genetic code. Enzymes that are mutated in some people with autism or related conditions attach the chemical tags to DNA. And that pattern of methyl marks across the genome can influence which genes are active or inactive at any given time. Much remains to be understood about this process, called DNA methylation. Here we describe how and when methylation happens and what researchers know about its relationship to autism. What is methylation? Methylation is the process by which enzymes called methyltransferases deposit methyl chemical groups onto DNA. The presence of these tags usually turns off nearby genes. The complete set of such modifications to the genome over a person’s lifetime is known as the methylome. Most methyl tags are deposited onto the DNA nucleotide called cytosine (C) whenever it occurs next to the nucleotide guanine (G). This CpG methylation begins during gestation and can change across the lifespan. Tags are also sometimes added to cytosines followed by other nucleotides, however. High levels of non-CpG methylation in the brain may be critical for neuron development. 2021 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 28115 - Posted: 12.15.2021

Mitch Leslie Medicine so far has nothing to offer that clearly prevents Alzheimer’s disease, although keeping your weight down, exercising regularly, and inheriting certain protective genes can lower your risk. Now, a study has identified another, unexpected source of protection: clonal hematopoiesis, a blood cell imbalance best known as a risk factor for cancer and heart disease. “Clonal hematopoiesis has been associated with so many bad outcomes that it is surprising that it is protective in this situation,” says cardiovascular biologist Kenneth Walsh of the University of Virginia, who wasn’t connected to the study, reported on 12 December at the American Society of Hematology meeting in Atlanta. But Walsh says the work is convincing and “will have to be reckoned with and explained.” He and other researchers caution that the discovery doesn’t offer any immediate opportunities for treating or preventing Alzheimer’s disease. Given the negative health effects of clonal hematopoiesis, inducing it in healthy people is a nonstarter. Still, the finding has a provocative implication: that cells from the bloodstream are restocking the brain’s immune cells, perhaps bolstering its ability to clear out toxic debris. Charles Darwin probably never imagined that natural selection unfolds in our bone marrow. But clonal hematopoiesis results from competition among the 50,000 to 200,000 stem cells that dwell there and divide to produce all our red and white blood cells. Over the years these stem cells accrue mutations, some of which result in a “fitter” cell whose progeny, known collectively as a clone, can soon outnumber their counterparts. In some people with clonal hematopoiesis, the offspring of a single mutated stem cell account for more than half of the blood cells in the body. © 2021 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 28114 - Posted: 12.15.2021

By Lisa Sanders, M.D. The 66-year-old man had just started his third lap at the community swimming pool outside Poughkeepsie, N.Y., when it struck. As he was turning his head to take a breath, an octopus of pain wrapped around the right side of his skull, starting at the joint where the jaw connects and slamming across his face and head with tentacles of squeezing agony. For a moment he was paralyzed — first with pain, then with fear. He couldn’t breathe; he could barely move. He struggled to the side of the pool and hung on, his breath ragged through involuntarily clenched teeth. His wife hurried over. He was a good swimmer; what was wrong? She saw his lips move and leaned closer. His jaw was clenched. “I can’t speak,” he mumbled. She helped him out of the pool. “We’re going to go to urgent care,” she said as she handed him a towel. These strange pains had been tormenting the man for nearly three weeks. It started as a headache that woke him from a dead sleep, a squeezing pressure deep inside his brain. He got up and took some acetaminophen. When he awoke the next morning, the headache was gone, but the regions around his head and face where the pressure had been strongest felt strangely tender. He couldn’t even brush his hair on the right side of his head. Bizarre as this was, he most likely would have soon forgotten about it except that it happened again the next night — and just about every night since. The pain in his jaw started a couple of days later. Opening and closing his mouth, and especially chewing, made his jaw throb. Eating anything more solid than mashed potatoes triggered excruciating pain. He went to his dentist, who poked and prodded. The only tenderness was in the joint where the jaw attached to the skull. It’s most likely TMJ, the dentist concluded — temporomandibular joint pain. That joint and the many attached muscles make speech and facial expressions possible. Lots of people have pain there, the dentist added. Bad habits like jaw-clenching and tooth-grinding aggravate the joint. The treatment is behavior modification to unlearn these habits, and sometimes a bite block, a custom-made piece of acrylic worn at night to protect teeth from injury. © 2021 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28113 - Posted: 12.15.2021

Jeanne Paz Blocking an immune system molecule that accumulates after traumatic brain injury could significantly reduce the injury’s detrimental effects, according to a recent mouse study my neuroscience lab and I published in the journal Science. The cerebral cortex, the part of the brain involved in thinking, memory and language, is often the primary site of head injury because it sits directly beneath the skull. However, we found that another region near the center of the brain that regulates sleep and attention, the thalamus, was even more damaged than the cortex months after the injury. This may be due to increased levels of a molecule called C1q, which triggers a part of the immune system called the classical complement pathway. This pathway plays a key role in rapidly clearing pathogens and dead cells from the body and helps control the inflammatory immune response. C1q plays both helpful and harmful roles in the brain. On the one hand, accumulation of C1q in the brain can trigger abnormal elimination of synapses – the structures that allow neurons to communicate with one another – and contribute to neurodegenerative disease. On the other hand, C1q is also involved in normal brain development and protects the central nervous system from infection. In the case of traumatic brain injury, we found that C1q lingered in the thalamus at abnormally high levels for months after the initial injury and was associated with inflammation, dysfunctional brain circuits and neuronal death. This suggests that higher levels of C1q in the thalamus could contribute to several long-term effects of traumatic brain injury, such as sleep disruption and epilepsy. © 2010–2021, The Conversation US, Inc.

Keyword: Brain Injury/Concussion; Neuroimmunology
Link ID: 28112 - Posted: 12.15.2021

By Bruce Bower Evidence that cross-continental Stone Age networking events powered human evolution ramped up in 2021. A long-standing argument that Homo sapiens originated in East Africa before moving elsewhere and replacing Eurasian Homo species such as Neandertals has come under increasing fire over the last decade. Research this year supported an alternative scenario in which H. sapiens evolved across vast geographic expanses, first within Africa and later outside it. The process would have worked as follows: Many Homo groups lived during a period known as the Middle Pleistocene, about 789,000 to 130,000 years ago, and were too closely related to have been distinct species. These groups would have occasionally mated with each other while traveling through Africa, Asia and Europe. A variety of skeletal variations on a human theme emerged among far-flung communities. Human anatomy and DNA today include remnants of that complex networking legacy, proponents of this scenario say. It’s not clear precisely how often or when during this period groups may have mixed and mingled. But in this framework, no clear genetic or physical dividing line separated Middle Pleistocene folks usually classed as H. sapiens from Neandertals, Denisovans and other ancient Homo populations. “Middle Pleistocene Homo groups were humans,” says paleoanthropologist John Hawks of the University of Wisconsin–Madison. “Today’s humans are a remix of those ancient ancestors.” © Society for Science & the Public 2000–2021.

Keyword: Evolution; Sexual Behavior
Link ID: 28111 - Posted: 12.15.2021

By Gretchen Reynolds Many of us remember “The Biggest Loser,” the somewhat notorious reality television show that ran for more than a decade starting in 2004, in which contestants competed feverishly to drop massive amounts of weight over a short period of time. One of the biggest lessons of the show appeared to be that extreme exercise, along with draconian calorie restriction, would lead to enormous weight loss. Media coverage of the contestants years later, though, seemed to tell a different story, of weight regain and slowed metabolisms and the futility of attempting long-term weight loss. Now a new scientific analysis of the show and its aftermath, published last month in the journal Obesity, suggests many beliefs about “The Biggest Loser” may be misconceptions. The analysis tries to untangle what really happened to the contestants’ metabolisms and why some of them kept off weight better than others. It also looks into the complex role of exercise and whether staying physically active helped the contestants keep their weight under control for years, or not. For those who may have forgotten, or tried to, “The Biggest Loser” ran on NBC to generally high ratings for more than a dozen seasons. Contestants competed to drop the most pounds using extreme calorie restriction and hours of daily strenuous exercise. “Winners” typically shed hundreds of pounds in a few months. Such rapid and extreme weight loss caught the attention of Kevin Hall, a senior investigator at the National Institute of Diabetes and Digestive and Kidney Diseases, which is part of the National Institutes of Health. An expert on metabolism, Dr. Hall knew that when people drop lots of weight in a short period of time, they typically send their resting metabolic rates — the baseline calories we burn every day just by being alive — into free-fall. A lower resting metabolic rate can mean we burn fewer calories over all. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 28110 - Posted: 12.15.2021

By Erin Blakemore Anger — such as road rage and the simmering displeasure of the ongoing pandemic — is the watchword for 2021. But be careful — those big emotions could trigger a stroke. FAQ: What to know about the omicron variant of the coronavirus Researchers in a global study devoted to figuring out stroke triggers found that about 1 in 11 stroke patients experience anger or emotional upset in the hour before their stroke symptoms begin. The study, published in the European Heart Journal, looked at data from 13,462 patients in 32 countries who had strokes. The patients completed extensive questionnaires during the first three days after they were hospitalized, answering questions about their medical history and what they had been doing and feeling before their stroke. Just over 8 percent of the patients surveyed said they had experienced anger or emotional upset within a day of symptom onset, which served as the control period. Just over 9 percent said they had been angry or upset within an hour of the first symptoms of their stroke, which was the test period. The risk of a stroke was higher in the test period when compared with the control period, the researchers said. “Our research found that anger or emotional upset was linked to an approximately 30% increase in risk of stroke during one hour after an episode — with a greater increase if the patient did not have a history of depression,” Andrew Smyth, a professor of clinical epidemiology at NUI Galway in Ireland who co-led the study, said in a statement. Lower education upped the odds of having a stroke linked with anger or emotional upset, as well.

Keyword: Stroke; Emotions
Link ID: 28109 - Posted: 12.15.2021

By Pam Belluck What if something in the blood of an athlete could boost the brainpower of someone who doesn’t or can’t exercise? Could a protein that gets amplified when people exercise help stave off symptoms of Alzheimer’s and other memory disorders? That’s the tantalizing prospect raised by a new study in which researchers injected sedentary mice with blood from mice that ran for miles on exercise wheels, and found that the sedentary mice then did better on tests of learning and memory. The study, published Wednesday in the journal Nature, also found that the type of brain inflammation involved in Alzheimer’s and other neurological disorders was reduced in sedentary mice after they received their athletic counterparts’ blood. “We’re seeing an increasing number of studies where proteins from outside the brain that are made when you exercise get into the brain and are helpful for improving brain health, or even improving cognition and disease,” said Rudolph Tanzi, a professor of neurology at Massachusetts General Hospital and Harvard Medical School. He led a 2018 study that found that exercise helped the brains of mice engineered to have a version of Alzheimer’s. The most promising outcome would be if exercise-generated proteins can become the basis for treatments, experts said. The study, led by researchers at Stanford School of Medicine, found that one protein — clusterin, produced in the liver and in heart muscle cells — seemed to account for most of the anti-inflammatory effects. But several experts noted that recent studies have found benefits from other proteins. They also said more needs to be learned about clusterin, which plays a role in many diseases, including cancer, and may have negative effects in early stages of Alzheimer’s before brain inflammation becomes dominant. © 2021 The New York Times Company

Keyword: Alzheimers; Hormones & Behavior
Link ID: 28108 - Posted: 12.11.2021

By Dr Lisa Feldman-Barrett The question of free will is still hotly debated. On the one hand, we clearly experience ourselves as able to make choices and freely act on them. If you fancy some crisps, you can choose to walk into a shop, buy a packet and eat them. Or you can choose to eat a pastry, a salad, or nothing at all. This certainly feels like free will. On the other hand, neuroscience evidence clearly shows that the brain usually initiates our actions before we’re aware of them. Here’s what I mean. Your brain’s primary task is to regulate the systems of your body to keep you alive and well. But there’s a snag: your brain spends its days locked in a dark, silent box (your skull) with no direct access to what’s going on inside your body or outside in the world. It receives ongoing information about the state of your body and the world – ‘sense data’– from the sensory surfaces of your body (your retina in your eyes, your cochlea in your ears, and so on). These sense data are outcomes of events in the world and inside your body. But your brain does not have access to the events or their causes. It only receives the outcomes. A loud bang, for example, might be thunder, a gunshot, or a drum, and each possible cause means different actions for your brain to launch. How does your brain figure out the causes of sense data, so that it prepares the best actions? Without direct access to those causes, your brain has to guess. And so, in every moment, your brain remembers past experiences that are similar to your present circumstances, to guess what might happen in the next moment, so it can prepare your body’s next action.

Keyword: Consciousness
Link ID: 28107 - Posted: 12.11.2021

Sofia Moutinho When Thomas Edison hit a wall with his inventions, he would nap in an armchair while holding a steel ball. As he started to fall asleep and his muscles relaxed, the ball would strike the floor, waking him with insights into his problems. Or so the story goes. Now, more than 100 years later, scientists have repeated the trick in a lab, revealing that the famous inventor was on to something. People following his recipe tripled their chances of solving a math problem. The trick was to wake up in the transition between sleep and wakefulness, just before deep sleep. “It is a wonderful study,” says Ken Paller, a cognitive neuroscientist at Northwestern University who was not part of the research. Prior work has shown that passing through deep sleep stages helps with creativity, he notes, but this is the first to explore in detail the sleep-onset period and its role in problem-solving. In this transitional period, we are not quite awake, but also not deeply asleep. It can be as short as a minute and occurs right when we start to doze off. Our muscles relax, and we have dreamlike visions or thoughts called hypnagogia, generally related to recent experiences. This phase slips by unnoticed most of the time unless it is interrupted by waking. Like Edison, surrealist painter Salvador Dalí believed interrupting sleep’s onset could boost creativity. (He used a heavy key instead of a metal ball.) To see whether Dalí and Edison were right, researchers recruited more than 100 easy sleepers. The team gave them a math test that required them to convert strings of eight digits into new strings of seven by using specific rules in a stepwise manner, such as “repeat the number if the previous and next digit are identical.” The volunteers weren’t told that there was an easier way to get the right answers by following a hidden rule: The second number in their final string was always the same as the last number in the same string. © 2021 American Association for the Advancement of Science.

Keyword: Sleep; Attention
Link ID: 28106 - Posted: 12.11.2021