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

Iris Berent How can a cellist play like an angel? Why am I engrossed in my book when others struggle with reading? And while we’re at it, can you tell me why my child won’t stop screaming? Now neuroscience offers the answers—or so say the news headlines. The brains of musicians “really do” differ from those of the rest of us. People with dyslexia have different neural connections than people without the condition. And your screaming toddler’s tantrums originate from her amygdala, a brain region linked to emotions. It’s all in the brain! Neuroscience is fascinating. But it is not just the love of science that kindles our interest in these stories. Few of us care for the technical details of how molecules and electrical charges inthe brain give rise to our mental life. Furthermore, invoking the brain does not always improve our understanding. You hardly need a brain scan to tell that your toddler is enraged. Nor is it surprising that an amateur cellist’s brain works differently than Yo-Yo Ma’s—or that the brains of typical and dyslexic readers differ in some way. Where else would those differences reside? These sorts of science news stories speak to a bias: As numerous experiments have demonstrated, we have a blind spot for the brain. In classic work on the “seductive allure of neuroscience,” a team of researchers at Yale University presented participants with a psychological phenomenon (for instance, children learning new words), along with two explanations. One invoked a psychological mechanism, and the other was identical except it also dropped in a mention of a brain region. The brain details were entirely superfluous—they did nothing to improve the explanation, as judged by neuroscientists. Yet laypeople thought they did, so much so that once the brain was invoked, participants overlooked gross logical flaws in the accounts. © 2021 Scientific American,

Keyword: Attention
Link ID: 28105 - Posted: 12.11.2021

Monique Brouillette Last summer a group of Harvard University neuroscientists and Google engineers released the first wiring diagram of a piece of the human brain. The tissue, about the size of a pinhead, had been preserved, stained with heavy metals, cut into 5,000 slices and imaged under an electron microscope. This cubic millimeter of tissue accounts for only one-millionth of the entire human brain. Yet the vast trove of data depicting it comprises 1.4 petabytes’ worth of brightly colored microscopy images of nerve cells, blood vessels and more. “It is like discovering a new continent,” said Jeff Lichtman of Harvard, the senior author of the paper that presented these results. He described a menagerie of puzzling features that his team had already spotted in the human tissue, including new types of cells never seen in other animals, such as neurons with axons that curl up and spiral atop each other and neurons with two axons instead of one. These findings just scratched the surface: To search the sample completely, he said, would be a task akin to driving every road in North America. Lichtman has spent his career creating and contemplating these kinds of neural wiring diagrams, or connectomes — comprehensive maps of all the neural connections within a part or the entirety of a living brain. Because a connectome underpins all the neural activity associated with a volume of brain matter, it is a key to understanding how its host thinks, feels, moves, remembers, perceives, and much more. Don’t expect a complete wiring diagram for a human brain anytime soon, however, because it’s technically infeasible: Lichtman points out that the zettabyte of data involved would be equivalent to a significant chunk of the entire world’s stored content today. In fact, the only species for which there is yet a comprehensive connectome is Caenorhabditis elegans, the humble roundworm. Nevertheless, the masses of connectome data that scientists have amassed from worms, flies, mice and humans are already having a potent effect on neuroscience. And because techniques for mapping brains are getting faster, Lichtman and other researchers are excited that large-scale connectomics — mapping and comparing the brains of many individuals of a species — is finally becoming a reality. Share this article Simons Foundation All Rights Reserved © 2021

Keyword: Brain imaging
Link ID: 28104 - Posted: 12.08.2021

by Anna Goshua Mice that lack one copy of TBX1, a gene in the autism-linked 22q11.2 chromosomal region, produce too little myelin — the fatty insulation that surrounds neurons — and perform poorly on tasks that measure cognitive speed, according to a new study. The work, published 5 November in Molecular Psychiatry, may offer insight into the mechanisms that underlie impaired cognitive function in some people with a 22q11.2 deletion, and possibly other copy number variants (CNVs). “The myelin changes could potentially emerge as a common neuronal deficit that mediates cognitive changes among many CNV cases,” says lead investigator Noboru Hiroi, professor of pharmacology at the University of Texas Health Science Center at San Antonio. Neuronal axons — the projections that conduct nerve impulses — are coated with myelin, which serves to speed up electrical transmission. The brains of autistic people and several mouse models of autism have disruptions in myelin, previous research has shown. These connecting fibers are the “highways of the brain,” says Valerie Bolivar, research scientist at the New York State Department of Health’s Wadsworth Center in Albany. “If the highway doesn’t work, you can’t get your goods from one place to another as fast.” TBX1 encodes a protein that regulates the expression of other genes during brain development. Deleting one copy of TBX1 leads to social and communication deficits in mice, according to previous studies by Hiroi’s team. © 2021 Simons Foundation

Keyword: Autism; Glia
Link ID: 28103 - Posted: 12.08.2021

By Elizabeth Preston A person trying to learn the way around a new neighborhood might spend time studying a map. You would probably not benefit from being carried rapidly through the air, upside-down in the dark. Yet that’s how some baby bats learn to navigate, according to a study published last month in Current Biology. As their mothers tote them on nightly trips between caves and certain trees, the bat pups gain the skills they need to get around when they grow up. Mothers of many bat species carry their young while flying, said Aya Goldshtein, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Konstanz, Germany. Egyptian fruit bats, for example, are attached to their mothers continuously for the first three weeks of life. While a mother searches for food, her pup clings to her body with two feet and its jaw, latching its teeth around her nipple. Mothers can still be seen flying with older pups that weigh 40 percent of what they do. It hadn’t been clear why the moms go to this length, instead of leaving pups in the cave where they roost, as some other species do. Dr. Goldshtein worked with Lee Harten, a behavioral ecologist at Tel Aviv University in Israel, where both she and Dr. Goldshtein were graduate students at the time in the lab of Yossi Yovel, a study co-author, to make sense of this maternal mystery. The researchers captured Egyptian fruit bat mothers and pups from a cave just outside Tel Aviv. They attached a tag holding a radio transmitter and miniature GPS device to each bat’s fur that would drop off after a couple of weeks. Then, the researchers brought the bats back to their cave. To track the bats, Dr. Harten held an antenna while standing on the roof of a 10-story building with a view of the cave. She directed Dr. Goldshtein, who was on foot or in a car with her own antenna, to follow the radio signals of bat pairs as they flew out at night. But again and again, there was a problem: The pup’s movement would suddenly stop, while the mother’s signal disappeared. “At the beginning we thought that we were doing our job wrong, and just losing the bats,” Dr. Harten said. © 2021 The New York Times Company

Keyword: Learning & Memory; Animal Migration
Link ID: 28102 - Posted: 12.08.2021

L. Carol Ritchie U.S. Surgeon General Vivek Murthy has a warning about the mental health of young people. Murthy told Morning Edition that children and young adults were already facing a mental health crisis before the coronavirus pandemic began: One in three high school students reported persistent feelings of sadness or hopelessness, a 40% increase from 2009 to 2019, he said. Suicide rates went up during that time by 57% among youth ages 10 to 24. During the pandemic, rates of anxiety and depression have increased, he said. The pandemic has made the issues behind the mental health crisis only worse, he said. "This is a critical issue that we have to do something about now," he said. "We can't wait until after the pandemic is over." Murthy, who issued an advisory called "Protecting Youth Mental Health," also cites gun violence, the specter of climate change, racism and social conflict as sources of stress. "We also have to recognize that kids increasingly are experiencing bullying, not just in school but online, that they're growing up in a popular culture and a media culture that reminds kids often that they aren't good-looking enough, thin enough, popular enough, rich enough, frankly, just not enough," he said. Article continues after sponsor message "Even to this day, even though I have parents who I know unconditionally loved me, I never felt comfortable telling them about it because I thought that this was my fault. I don't want that to be the reality for my children, who are 4 and 5 and growing up, you know, in this very complicated world." © 2021 npr

Keyword: Depression
Link ID: 28101 - Posted: 12.08.2021

Alison Abbott There Is Life After the Nobel Prize Eric Kandel Columbia Univ. Press (2021) In 1996, Denise Kandel warned her husband that were he to win the Nobel prize for his pioneering work on memory, then it should be later rather than sooner. Laureates too often turn into socialites, she warned, and stop contributing to the intellectual life of science. Just four years later, Eric Kandel shared the 2000 Nobel Prize in Physiology or Medicine. He was then 71, an age when he could legitimately have rested on his laurels. But resting is not among Kandel’s many strengths. His new book, There Is Life After the Nobel Prize, outlines his achievements of the past couple of decades — numerous enough to dispel Denise’s fears, he writes. It is hard to disagree. The volume adds to Kandel’s respected literary oeuvre, which ranges from neuroscience textbooks to highly original popular science. But it is slight, and feels like a coda. In it, he summarises his post-Nobel research (on learning and memory deficits in addiction, schizophrenia and ageing), writing and public outreach. And he acknowledges colleagues and sponsors of his long career, particularly the Howard Hughes Medical Institute in Chevy Chase, Maryland, and Columbia University in New York City, where he remains a professor and institute director. A fuller and more poignant autobiography can be found in Kandel’s 2006 book In Search of Memory. There, he explains why his traumatic childhood in Austria drew him to study the mechanisms of memory. That book also presents a marvellous history of neuroscience. Making sense Kandel was born in 1929 in Vienna. His family was Jewish and owned a toy shop. When Hitler annexed Austria in 1938, his parents began their year-long effort to emigrate. They finally arrived in New York shortly before the outbreak of World War II, physically unharmed but psychologically traumatized. © 2021 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 28100 - Posted: 12.08.2021

By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

Keyword: Depression; Drug Abuse
Link ID: 28099 - Posted: 12.04.2021

By Pam Belluck AURORA, Ill. — There is sobering evidence of Samantha Lewis’s struggle with long Covid on her bathroom mirror. Above the sink, she has posted a neon pink index card scrawled with nine steps (4. Wet brush 5. Toothpaste) reminding her how to brush and floss her teeth. It is one of many strategies Ms. Lewis, 34, has learned from “cognitive rehab,” an intensive therapy program for Covid-19 survivors whose lives have been upended by problems like brain fog, memory lapses, dizziness and debilitating fatigue. Nearly two years into the pandemic, advances have been made in treating Covid itself, but long Covid — a constellation of lingering health problems that some patients experience — remains little understood. Post-Covid clinics around the country are trying different approaches to help patients desperate for answers, but there is little data on outcomes so far, and doctors say it is too soon to know what might work, and for which patients. While some physical symptoms of long Covid, like shortness of breath or nausea, can be addressed with medication, cognitive issues are more challenging. Few drugs exist, and while some deficits can rebound with time, they can also be exacerbated by resuming activities too soon or intensively. Over several months, The New York Times visited Ms. Lewis, interviewed her doctors, attended her therapy sessions and read her medical records. Before she was infected with the coronavirus in October 2020, experiencing a modest initial illness that did not require hospitalization, she was successfully juggling a demanding, detail-oriented job while raising a child with autism and attention deficit hyperactivity disorder. But this summer, she scored 25 on a 30-point assessment, placing her in a pre-dementia category called mild cognitive impairment. © 2021 The New York Times Company

Keyword: Learning & Memory
Link ID: 28098 - Posted: 12.04.2021

By Bob Goldstein On a cold, dry Tuesday in December, 1940, Rita Levi-Montalcini rode a train from the station near her home in Turin, Italy, for 80 miles to Milan to buy a microscope. Milan had not seen bombings for months. On her return to the Turin train station, two police officers stopped her and demanded to see inside the cake-sized box that she was carrying. With wartime food rationing, panettone cakes were only available illegally. The officers found her new microscope instead. They let her go. Just a week after her trip, British bombers hit Milan. Levi-Montalcini was a 31-year-old scientist who had been working at the University of Turin. Despite her father’s disapproval, she had trained in medicine, inspired by seeing a nanny succumb to cancer. In 1938, the Italian dictator Mussolini banned Jews from positions in universities. Levi-Montalcini was not raised in the Jewish religion, but her Jewish ancestry would have been evident from her surname. Mussolini’s ban had pushed Levi-Montalcini to leave Italy for Belgium in 1939, where she did research using fertilized chicken eggs as a source of material for her research topic: the developing nervous systems of vertebrate embryos. Levi-Montalcini also spent time with her older sister Nina, whose family was in Belgium as well. Rita wrote home to her mother of an “infinite desire to embrace you again,” but research at the university in Turin would have been impossible had she returned home. Her passion for research alternated with her frustration with challenges. When Hitler invaded Poland in September, launching war, her worst frustrations were realized. The “whole world was in danger,” Levi-Montalcini later wrote. In December 1939, she returned to Italy. © 2021 NautilusThink Inc,

Keyword: Apoptosis; Development of the Brain
Link ID: 28097 - Posted: 12.04.2021

By Emily Cataneo If you could upload your consciousness to the cloud and live forever as a mind in the metaverse, would you do it? Think carefully before answering. In “Feeling & Knowing: Making Minds Conscious,” neuroscientist Antonio Damasio argues that consciousness is far more than an algorithmic process. Uploading your consciousness to the cloud, he says, would be like experiencing a meal by reading a recipe rather than by eating. So then what is consciousness? That’s the question at the heart of this book. Damasio is a professor of neuroscience, philosophy, and psychology and the director of the Brain and Creativity Institute at the University of Southern California, Los Angeles, as well as the author of the 2018 book “The Strange Order of Things,” in which he extols the power of homeostasis, the force that keeps all living beings in equilibrium and therefore alive. Consciousness is such a slippery and ephemeral concept that it doesn’t even have its own word in many Romance languages, but nevertheless it’s a hot topic these days. “Feeling & Knowing” is the result of Damasio’s editor’s request to weigh in on the subject by writing a very short, very focused book. Over 200 pages, Damasio ponders profound questions: How did we get here? How did we develop minds with mental maps, a constant stream of images, and memories — mechanisms that exist symbiotically with the feelings and sensations in our bodies that we then, crucially, relate back to ourselves and associate with a sense of personhood?

Keyword: Consciousness
Link ID: 28096 - Posted: 12.04.2021