By Rebecca Robbins The Food and Drug Administration on Friday called for a federal investigation of the process that led to the approval of a new drug for Alzheimer’s disease that has spurred sharp criticism from lawmakers and the medical community. In a letter to the Department of Health and Human Services’ independent Office of the Inspector General, the F.D.A.’s acting commissioner, Dr. Janet Woodcock, acknowledged the scrutiny the agency has faced about the approval process for the drug, which is known as Aduhelm and has a $56,000 annual price tag. She pointed to interactions between representatives from the drug’s developer, Biogen, and the agency, saying some “may have occurred outside of the formal correspondence process.” “To the extent these concerns could undermine the public’s confidence in F.D.A.’s decision, I believe it is critical that the events at issue be reviewed by an independent body,” Dr. Woodcock wrote. She noted that the review should look at whether any of the communication between the agency’s staff and Biogen’s representatives violated F.D.A. rules. Dana Conti, a spokesman for Biogen, said the company “will, of course, cooperate with any inquiry in connection with a possible review of the regulatory process.” It is unusual for the agency to request an investigation into its own staff’s decision-making process for an individual drug approval. The move is likely to intensify the controversy that has surrounded Aduhelm. The F.D.A. approved it a month ago, overriding the fierce objections of its own independent advisers and many other scientists, who said there was insufficient evidence to know whether the drug was effective. On Thursday, the F.D.A. moved to narrow its recommendation about who should receive the drug. After originally recommending it for all Alzheimer’s patients, the agency’s new guidelines say it should be prescribed only to people with mild cognitive problems. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 27900 - Posted: 07.10.2021

Michael Marshall Since the beginning of the pandemic, researchers have been trying to understand how the coronavirus SARS-CoV-2 affects the brain.Credit: Stanislav Krasilnikov/TASS/Getty How COVID-19 damages the brain is becoming clearer. New evidence suggests that the coronavirus’s assault on the brain could be multipronged: it might attack certain brain cells directly, reduce blood flow to brain tissue or trigger production of immune molecules that can harm brain cells. Infection with the coronavirus SARS-CoV-2 can cause memory loss, strokes and other effects on the brain. The question, says Serena Spudich, a neurologist at Yale University in New Haven, Connecticut, is: “Can we intervene early to address these abnormalities so that people don’t have long-term problems?” With so many people affected — neurological symptoms appeared in 80% of the people hospitalized with COVID-19 who were surveyed in one study1 — researchers hope that the growing evidence base will point the way to better treatments. Breaking into the brain SARS-CoV-2 can have severe effects: a preprint posted last month2 compared images of people’s brains from before and after they had COVID-19, and found loss of grey matter in several areas of the cerebral cortex. (Preprints are published without peer review.) Early in the pandemic, researchers speculated that the virus might cause damage by somehow entering the brain and infecting neurons, the cells responsible for transmitting and processing information. But studies have since indicated3 that the virus has difficulty getting past the brain’s defence system — the blood–brain barrier — and that it doesn’t necessarily attack neurons in any significant way.

Keyword: Chemical Senses (Smell & Taste); Learning & Memory
Link ID: 27899 - Posted: 07.08.2021

Elena Renken For decades, neuroscientists have treated the brain somewhat like a Geiger counter: The rate at which neurons fire is taken as a measure of activity, just as a Geiger counter’s click rate indicates the strength of radiation. But new research suggests the brain may be more like a musical instrument. When you play the piano, how often you hit the keys matters, but the precise timing of the notes is also essential to the melody. “It’s really important not just how many [neuron activations] occur, but when exactly they occur,” said Joshua Jacobs, a neuroscientist and biomedical engineer at Columbia University who reported new evidence for this claim last month in Cell. For the first time, Jacobs and two coauthors spied neurons in the human brain encoding spatial information through the timing, rather than rate, of their firing. This temporal firing phenomenon is well documented in certain brain areas of rats, but the new study and others suggest it might be far more widespread in mammalian brains. “The more we look for it, the more we see it,” Jacobs said. Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. Some researchers think the discovery might help solve a major mystery: how brains can learn so quickly. The phenomenon is called phase precession. It’s a relationship between the continuous rhythm of a brain wave — the overall ebb and flow of electrical signaling in an area of the brain — and the specific moments that neurons in that brain area activate. A theta brain wave, for instance, rises and falls in a consistent pattern over time, but neurons fire inconsistently, at different points on the wave’s trajectory. In this way, brain waves act like a clock, said one of the study’s coauthors, Salman Qasim, also of Columbia. They let neurons time their firings precisely so that they’ll land in range of other neurons’ firing — thereby forging connections between neurons. All Rights Reserved © 2021

Keyword: Brain imaging
Link ID: 27898 - Posted: 07.08.2021

By Elizabeth Pennisi Almost 200 years ago, the renowned U.S. naturalist John James Audubon hid a decaying pig carcass under a pile of brush to test vultures’ sense of smell. When the birds overlooked the pig—while one flocked to a nearly odorless stuffed deer skin—he took it as proof that they rely on vision, not smell, to find their food. His experiment cemented a commonly held idea. Despite later evidence that vultures and a few specialized avian hunters use odors after all, the dogma that most birds aren’t attuned to smell endured. Now, that dogma is being eroded by findings on birds’ behavior and molecular hardware, two of which were published just last month. One showed storks home in on the smell of freshly mowed grass; another documented scores of functional olfactory receptors in multiple bird species. Researchers are realizing, says evolutionary biologist Scott Edwards of Harvard University, that “olfaction has a lot of impact on different aspects of bird biology.” Forty years ago, when ethologist Floriano Papi proposed that homing pigeons find their way back to a roost by sniffing out its chemical signature, his colleagues scoffed at the idea. They pointed out that birds have several other keen senses to guide them, including sight and, in the case of pigeons and some other species, a magnetic sense. “By then, biological textbooks already stated unequivocally that birds have little to no sense of smell, and many people still believe it—even scientists,” says Danielle Whittaker, a chemical ecologist at Michigan State University. © 2021 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 27897 - Posted: 07.08.2021

Yuki Noguchi Health conditions exacerbated by obesity include heart disease, stroke, Type 2 diabetes and certain types of cancer, according to the CDC. Researchers say the newly approved drug Wegovy could help many who struggle with obesity lose weight. adamkaz/Getty Images When a promising new drug to treat obesity was approved by the Food and Drug Administration for sale in the U.S. last month, it was the first such treatment to gain approval since 2014. In clinical trials, weekly injections of semaglutide — or Wegovy, as it's been branded — helped people drop an average of 15% of their body weight. That's an average of about 34 pounds over 16 months, before their weight plateaued — roughly triple what's achieved with other drugs on the market. At least as important, Wegovy raised none of the alarm bells with the FDA or obesity doctors that it might trigger serious side effects of the sort some people experienced by taking fen-phen or other previous medical treatments for obesity. But with a price tag for Wegovy of $1,000 to $1,500 a month, a big question remains: Will insurers cover its significant cost for the millions such as Marleen Greenleaf who might benefit? Greenleaf grew up on the island of Trinidad, where her family paid little heed to what they ate and paid a high medical price, she says: "My husband has diabetes, my sister has diabetes, my brother has diabetes." Since then, she's tried — and failed — at numerous diets, says Greenleaf, now 58 and an administrator at a charter school in Washington, D.C. Then, in 2018, she signed up for the clinical trial of a new drug — a once-weekly shot that changes the way her brain signals hunger. © 2021 npr

Keyword: Obesity
Link ID: 27896 - Posted: 07.08.2021

By Laura Sanders A brush with death led Hans Berger to invent a machine that could eavesdrop on the brain. In 1893, when he was 19, Berger fell off his horse during maneuvers training with the German military and was nearly trampled. On that same day, his sister, far away, got a bad feeling about Hans. She talked her father into sending a telegram asking if everything was all right. To young Berger, this eerie timing was no coincidence: It was a case of “spontaneous telepathy,” he later wrote. Hans was convinced that he had transmitted his thoughts of mortal fear to his sister — somehow. So he decided to study psychiatry, beginning a quest to uncover how thoughts could travel between people. Chasing after a scientific basis for telepathy was a dead end, of course. But in the attempt, Berger ended up making a key contribution to modern medicine and science: He invented the electroencephalogram, or EEG, a device that could read the brain’s electrical activity. Berger’s machine, first used successfully in 1924, produced a readout of squiggles that represented the electricity created by collections of firing nerve cells in the brain. © Society for Science & the Public 2000–2021.

Keyword: Sleep
Link ID: 27895 - Posted: 07.08.2021

By Paula Span Dr. Kenneth Koncilja, a geriatrician at the Cleveland Clinic, saw the announcement from the Food and Drug Administration on June 7, on Twitter: The agency had approved Aduhelm (aducanumab), the first drug to treat Alzheimer’s disease to be approved in nearly 20 years. The calls from patients’ spouses and family members began within the hour, and have not stopped. “I was shocked at how fast the word spread — ‘Hey, is this something we can use? When can we get it?’” Dr. Koncilja recalled. “There’s a mix of excitement, anxiety and desperation.” His first call that morning came from Joan Morehouse, 78, who has been caring for her 71-year-old husband, James, in their home in North Perry, Ohio, since his Alzheimer’s diagnosis four years ago. She has watched him get lost on familiar drives and forget their grandchildren’s names. When her brother and her son both emailed her a news article about the F.D.A. action, she recalled, “I said, ‘Oh, my God, my prayers have been answered.’” It fell to Dr. Koncilja to explain the complexities: That Aduhelm is not yet widely available. That protocols determining which patients qualify have yet to be developed. That the clinical trial data was ambiguous and that the drug might bring no noticeable improvements in daily life. That its side effects include brain swelling and bleeding. And that its maker, Biogen, estimates the annual cost of monthly intravenous infusions at $56,000, plus expensive scans and tests. “It’s a more difficult question than I’ve ever had before,” Dr. Koncilja said. Patients ask him how their lives will change, “and I don’t know how to answer.” © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 27894 - Posted: 07.08.2021

By Jane E. Brody I was doing research and interviews on bipolar disorder when notices appeared in my Brooklyn neighborhood about a 21-year-old man who had been missing for a week. He was described as “bipolar” and “may be experiencing a manic episode.” It took me back nearly seven decades when the state police in Texas called my father to say they had found his brother, my favorite uncle, wandering on a highway. How he got there from Brooklyn we never learned. He had apparently suffered a psychotic break and ended up in a New York State mental hospital that administered electric shock treatments but did little else to help him re-enter society effectively. Not until decades later did he receive a correct diagnosis of manic depression, now known as bipolar disorder. Characterized by extreme shifts in mood, “manic-depressive illness” was officially recognized by the American Psychiatric Association in 1952. But it would be many years before an effective treatment, the drug lithium, which acts on the brain to help stabilize debilitating episodes of severe mania and depression, was available to help my brilliant uncle resume a reasonably normal life. Bipolar disorder typically runs in families, with different members experiencing symptoms to a greater or lesser degree. If a parent has the disorder, a child’s risk can rise to 10 percent. My uncle’s only child displayed some minor behavioral characteristics of bipolar disorder, like very rapid speech and frenetic activity, but was able to complete two advanced degrees, marry, be a parent and succeed in an intellectually demanding career. Bipolar disorder is most often diagnosed in the later teen years or young adulthood, affecting some 4 percent of people at some point in their lives. But in recent decades, diagnosis of the disorder has soared in children and adolescents, although some experts believe the condition is overdiagnosed or overtreated with potent psychiatric drugs. © 2021 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 27893 - Posted: 07.06.2021

By Marlene Cimons J. William Langston, who has been studying and treating Parkinson’s disease for nearly 40 years, always has found it striking that so many more men than women show up in his clinic. His observation is not anecdotal. It is grounded in science and shared by many physicians: Men are roughly 1.5 times more likely than women to develop Parkinson’s, a progressive disorder of the nervous system that impairs movement and can erode mental acuity. “It’s a big difference that is quite real,” says Langston, clinical professor of neurology, neuroscience and of pathology at the Stanford University School of Medicine and associate director of the Stanford Udall Center. “It’s pretty dramatic. I think anyone who sees a lot of Parkinson’s will tell you that.” While the disproportionate impact is clear, the reasons for it are not. “It’s a great mystery,” Langston says. Researchers still don’t know what it is that makes men more susceptible to Parkinson’s, or what it is about women that may protect them — or both. But they are trying to find out. “We in the research community have been working for decades to sort this out, but the answers are still elusive,” says Caroline Tanner, a neurology professor in the Weill Institute for Neurosciences at the University of California at San Francisco. “Nevertheless, it’s important to keep at it. We need to understand the mechanisms that underlie the specific differences between men and women so we can apply them to trying to prevent Parkinson’s.” Parkinson’s results from the death of key neurons in the substantia nigra region of the brain that produce the chemical messenger dopamine. Over time, the loss of these nerve cells disrupts movement, diminishes cognition, and can cause other symptoms, such as slurred speech and depression. © 1996-2021 The Washington Post

Keyword: Parkinsons; Sexual Behavior
Link ID: 27892 - Posted: 07.06.2021

by Giorgia Guglielmi Autism research has long focused on genes involved in the formation of neurons and the function of synapses. Mutations in these genes were the first to be solidly linked to the condition and its traits. Over the past decade, however, several studies have implicated a second class of genes: those involved in the remodeling of chromatin — the complex of DNA and proteins that makes up chromosomes. These ‘chromatin regulators,’ which can influence whether other genes are turned on or off, are sometimes mutated in people with autism or other neurodevelopmental conditions. Scientists are just beginning to understand how these mutations can alter brain development. Why is chromatin remodeling important? If the chromosomes of a single human cell were stretched out and joined together end to end, their DNA would measure about 6.5 feet long. To fit inside a nucleus no wider than one-tenth of a human hair, the DNA strand wraps around histone proteins to form a series of bead-like structures called nucleosomes. Together these beads make up the chromatin. When a stretch of DNA is tightly packed into a nucleosome, it is inaccessible to the proteins that turn genes on and off by way of a process called transcription. For cells to express the right genes at the right time, their DNA needs to transition from tightly to loosely packed coils, a process carried out by a group of proteins called chromatin remodeling complexes. © 2021 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 27891 - Posted: 07.06.2021

By Laurie McGinley Neurologist Matthew S. Schrag was surprised when he heard the Food and Drug Administration had approved a controversial Alzheimer’s drug. There was scant evidence the treatment worked, in his view. Even more concerning to Schrag: the FDA’s apparent embrace of a long-debated theory about Alzheimer’s disease, which afflicts more than 6 million Americans. The amyloid hypothesis, which has dominated the field for decades, holds that toxic clumps in the brain, called amyloid beta, are the main driver of the disease and that removing them will slow cognitive decline. But years of testing drugs that target amyloid had yielded a string of failures, and Schrag and others had been pushing the field to focus on other possible factors, including inflammation in the brain or damage to tiny blood vessels. Anti-amyloid efforts, they said, had squeezed out other approaches that might be more promising. “We had been hoping for a recalibration of the field,” said Schrag, a researcher at Vanderbilt University Medical Center. Now, he’s worried drug companies will double down on an approach he thinks is a dead end. The role of the sticky clumps of protein in the brain has long divided researchers and is at the forefront again amid the FDA’s recent clearance of the first drug to treat the disease in almost two decades. It is one of many controversies that has erupted since the FDA approved the drug, called Aduhelm, on June 7. Members of Congress have vowed to conduct hearings on the relationship between the FDA and the drug’s maker, Massachusetts-based Biogen. Analysts worry the drug’s list price — $56,000 a year per patient — could wreck Medicare’s finances. Doctors are scrambling to decide who should take it, complaining that the FDA-approved label, which includes all Alzheimer’s patients, is far too broad.

Keyword: Alzheimers
Link ID: 27890 - Posted: 07.06.2021

By Sheila Kaplan Sales have plunged by $500 million. The work force has been cut by three-quarters. Operations in 14 countries have been abandoned. Many state and local lobbying campaigns have been shut down. Juul Labs, the once high-flying e-cigarette company that became a public health villain to many people over its role in the teenage vaping surge, has been operating as a shadow of its former self, spending the pandemic largely out of the public eye in what it calls “reset” mode. Now its very survival is at stake as it mounts an all-out campaign to persuade the Food and Drug Administration to allow it to continue to sell its products in the United States. The agency is trying to meet a Sept. 9 deadline to decide whether Juul’s devices and nicotine pods have enough public health benefit as a safer alternative for smokers to stay on the market, despite their popularity with young people who never smoked but became addicted to nicotine after using Juul products. Major health organizations, including the American Heart Association, American Lung Association, American Academy of Pediatrics and the American Cancer Society’s Cancer Action Network, have asked the agency to reject Juul’s application. “The stakes are high,” said Eric Lindblom, a senior scholar at the O’Neill Institute for National and Global Health Law at Georgetown University, and a former F.D.A. adviser on tobacco. “If the F.D.A. blows it on this one, they will face public health lawsuits.” Juul is sparing no expense to push back. Last week, the company agreed to pay $40 million to settle just one lawsuit (with North Carolina) out of thousands lodged against it, avoiding a looming jury trial. The company had urgently sought the deal to avoid courtroom testimony from parents and teenagers while the F.D.A. is reviewing its vaping products. © 2021 The New York Times Company

Keyword: Drug Abuse
Link ID: 27889 - Posted: 07.06.2021

Linda Geddes Science correspondent Fibromyalgia – a poorly understood condition that causes widespread pain throughout the body and extreme tiredness – may be caused by be an autoimmune response that increases the activity of pain-sensing nerves throughout the body. The findings, published in the Journal of Clinical Investigation, challenge the widely held view that the condition originates in the brain, and could pave the way for more effective treatments for the millions of people affected. They could also have implications for patients suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and “long Covid”. “These different syndromes are symptomatically very similar, so I think it could be very relevant to both of these conditions,” said Dr David Andersson from the Institute of Psychiatry, Psychology and Neuroscience at King’s College London, who led the new study. Fibromyalgia affects at least 1 in 40 people worldwide, although some estimates suggest nearly 1 in 20 people may be affected to some degree. It is characterised by widespread pain and crippling fatigue – often referred to as “fibro fog” – and usually develops between the ages of 25 and 55, although children can also get it. Similar to many autoimmune conditions, the vast majority of those affected (80% are women). Current treatment tends to focus on gentle aerobic exercise, as well as drug and psychological therapies designed to manage pain. However, these have proven ineffective in most patients and have left behind an enormous unmet clinical need, said Andersson. “The widespread paradigm at the moment is that this is a disease that emanates from the brain, and I think our findings suggest that that’s not the case,” he said. © 2021 Guardian News & Media Limited

Keyword: Neuroimmunology; Depression
Link ID: 27888 - Posted: 07.03.2021

By Rodrigo Pérez Ortega For some people, no amount of exercise and dieting keeps the kilograms off. For others, leanness comes naturally. Now, scientists might know one reason why. In one of the most comprehensive studies of the genetics of obesity to date, a research team has identified rare gene variants that protect lucky carriers from putting on weight. The work is “a tour de force of genetics,” says Sadaf Farooqi, an obesity researcher at the University of Cambridge who was not involved with the study. Geneticists generally look for mutations that cause disease, but people can also carry subtly different versions of a gene that promote good health. Finding rare variants that offer protection against a disease is very hard because sequencing studies are usually small, Farooqi notes. Yet such variants can lead to new drug targets, she adds. At least 2.8 million people die every year from being overweight or clinically obese. Obesity increases the risk of developing type 2 diabetes, heart disease, some cancers, and even severe COVID-19. Diet and exercise can help people with obesity lose weight, but genetics also strongly influence whether a person develops the disease. Studies that focused on people with extreme obesity have identified common gene variants—like a “broken” copy of the MC4R gene, linked to appetite regulation—that make people more likely to be overweight. Other work has found thousands of genetic variants, each of which has a tiny impact on body weight; together, they can significantly increase the likelihood of obesity. In the new study, researchers sequenced the genomes of more than 640,000 people from Mexico, the United States, and the United Kingdom, homing in on only the exome—the part of the genome that codes for proteins. © 2021 American Association for the Advancement of Science.

Keyword: Obesity; Genes & Behavior
Link ID: 27887 - Posted: 07.03.2021

Philip M. Boffey I was astonished to learn while writing a column on the brain-computer interface in 2019 that patients with amyotrophic lateral sclerosis (ALS), whose brain signals were fed into a computer, could control a complex robotic arm, having it pick up a pitcher and pour water into a glass, just by thinking about it. So you can imagine my surprise when I learned that scientists have achieved comparably difficult tasks—not with signals from a human brain—but simply from a clump of stem calls in a Petri dish. The achievement is clearly described in Alan Alda’s Clear+Vivid podcast featuring Alysson Muotri, a Brazilian citizen who is director of the stem cell program at University of California, San Diego, where much of this pioneering work was performed. The podcast is a useful complement to a more comprehensive report issued on April 8 by the National Academies of Sciences, Engineering, and Medicine. As Alda’s introduction explains, Muotri uses factors that drive skin cells to revert to stem cells and then become brain tissues that self-organize, forming “brain organoids in a dish. Muotri, who has a personal interest because he has a son with autism, hopes to learn how early brain development can change course in conditions like autism and epilepsy—and how our brains differ from those of our evolutionary? cousins, the Neanderthals. Although some people call what he has created “brains” or “mini-brains” in a dish, Muotri is more circumspect, describing them as “brain organoids.” © 2021 The Dana Foundation.

Keyword: Development of the Brain
Link ID: 27886 - Posted: 07.03.2021

Christopher McDermott, MBChB, FRCP, PhD Early in my clinical practice, my team and I subscribed to the traditional view of ALS: the disease was either familial or sporadic. People with “familial” ALS had some family history of ALS (and therefore a possible genetic component), while people with “sporadic” disease did not have a family history.1 But that view began to change with the discovery that mutations (or changes) in a gene called C9orf72 could play a role in both the sporadic and familial types of ALS. Over time, we learned that this one mutation accounted for approximately 40% of familial ALS cases. Even more surprising: it accounted for close to 10% of cases in people with no family history of ALS—people previously believed to have the sporadic form of the disease. As this story unfolded, we began to question our old assumptions about familial and sporadic ALS, and we realized that just asking our patients about their family history wasn’t enough. C9orf72 has been associated with other neurologic diseases as well, so now, I and other ALS specialists understood that someone with a family history of related conditions might also have a genetic cause for their ALS. At the same time, other genetic mutations were being found in people with no family history of the disease and whose ALS had seemingly appeared out of nowhere.1 It was becoming clear that some people with what we often referred to as sporadic ALS could actually have a genetic component to their disease.1 My own research supported this belief. The Sheffield Institute for Translational Neuroscience, where we help develop and study new therapies for neuromuscular diseases, had an extensive biobank of samples from people with ALS. As new genetic mutations were discovered, our researchers tested these samples and found that many people who we thought had sporadic ALS in fact had one or more genetic mutations. © 2013-2021 All rights reserved.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 27885 - Posted: 07.03.2021

Asher Mullard The recent controversial approval of the Alzheimer’s drug aducanumab by the US Food and Drug Administration (FDA) has raised the possibility that the agency could now be more willing to fast-track treatments for a swathe of neurodegenerative diseases — illnesses that have so far thwarted drug developers. But an independent advisory panel fiercely questioned the new drug’s effectiveness, and researchers are divided on whether the potentially smoother approval path that aducanumab has paved will really deliver useful therapies for people with conditions such as amyotrophic lateral sclerosis (ALS), Huntington’s disease and Parkinson’s disease. Drug developers including Amgen, in Thousand Oaks, California, and Pfizer, based in New York City, have shut down their neuroscience programmes in recent years because of the difficulties of finding successful treatments for brain diseases. So Eric Siemers, a drug-development consultant in Zionsville, Indiana, thinks aducanumab’s approval could bring renewed investment and innovation. On the basis of conversations he has had with investors and clients, he says the tide is already turning. “There’s a lot more interest now in research in neurodegenerative diseases,” says Siemers, who is also chief medical officer of the Alzheimer’s disease company Acumen Pharmaceuticals in Charlottesville, Virginia. Acumen filed paperwork for an initial public offering just days after the approval of aducanumab. Some advocacy groups are also encouraged, on behalf of desperate patients with few or no therapeutic options. “If the FDA can find a way to be flexible for Alzheimer’s, maybe they can find a way to be flexible for ALS,” says Neil Thakur, chief mission officer at the ALS Association. © 2021 Springer Nature Limited

Keyword: Alzheimers
Link ID: 27884 - Posted: 07.03.2021

By Anil Ananthaswamy “Everything became imbued with a sense of vitality and life and vividness. If I picked up a pebble from the beach, it would move. It would glisten and gleam and sparkle and be absolutely captivating,” says neuroscientist Anil Seth. “Somebody looking at me would see me staring at a stone for hours.” Or what seemed like hours to Seth. A researcher at the UK’s University of Sussex, he studies how the brain helps us perceive the world within and without, and is intrigued by what psychedelics such as LSD can tell us about how the brain creates these perceptions. So a few years ago, he decided to try some, in controlled doses and with trusted people by his side. He had a notebook to keep track of his experiences. “I didn’t write very much in the notebook,” he says, laughing. Instead, while on LSD, he reveled in a sense of well-being and marveled at the “fluidity of time and space.” He found himself staring at clouds and seeing them change into faces of people he was thinking of. If his attention drifted, the clouds morphed into animals. Seth went on to try ayahuasca, a hallucinogenic brew made from a shrub and a vine native to South America and often used in shamanistic rituals there. This time, he had a more emotional trip that dredged up powerful memories. Both experiences strengthened Seth’s conviction that psychedelics have great potential for teaching us about the inner workings of the brain that give rise to our perceptions. He’s not alone. Armed with fMRI scans, EEG recordings, computational models of the brain and reports from volunteers tripping on psychedelics, a small but growing number of neuroscientists are trying to take advantage of these drugs and the hallucinations they induce to better understand how the brain produces perceptions. © 2021 Annual Reviews, Inc

Keyword: Drug Abuse; Vision
Link ID: 27883 - Posted: 06.29.2021

By Emily Conover Scientists could be a step closer to understanding how some birds might exploit quantum physics to navigate. Researchers suspect that some songbirds use a “quantum compass” that senses the Earth’s magnetic field, helping them tell north from south during their annual migrations (SN: 4/3/18). New measurements support the idea that a protein in birds’ eyes called cryptochrome 4, or CRY4, could serve as a magnetic sensor. That protein’s magnetic sensitivity is thought to rely on quantum mechanics, the math that describes physical processes on the scale of atoms and electrons (SN: 6/27/16). If the idea is shown to be correct, it would be a step forward for biophysicists who want to understand how and when quantum principles can become important in various biological processes. In laboratory experiments, the type of CRY4 in retinas of European robins (Erithacus rubecula) responded to magnetic fields, researchers report in the June 24 Nature. That’s a crucial property for it to serve as a compass. “This is the first paper that actually shows that birds’ cryptochrome 4 is magnetically sensitive,” says sensory biologist Rachel Muheim of Lund University in Sweden, who was not involved with the research. Scientists think that the magnetic sensing abilities of CRY4 are initiated when blue light hits the protein. That light sets off a series of reactions that shuttle around an electron, resulting in two unpaired electrons in different parts of the protein. Those lone electrons behave like tiny magnets, thanks to a quantum property of the electrons called spin. © Society for Science & the Public 2000–2021.

Keyword: Animal Migration; Vision
Link ID: 27882 - Posted: 06.29.2021

By Katherine Ellison Remember the line from that old folk song? If living were a thing that money could buy You know the rich would live and the poor would die. Sadly, there’s little “if” about it. On average, the poor live less healthy lives and are more than three times as likely to die prematurely as the rich. That’s true for many well-documented reasons, including less healthy diets with too much processed food, polluted neighborhoods and a lot more toxic stress. In recent years, however, researchers have added one more factor to this mix: It turns out that the poor, as well as socially disadvantaged racial minorities, sleep much less well on average than the rich, which can take a major toll on their physical and mental health. “We used to think that sleep problems were limited to Type A professionals, and they certainly aren’t immune, but low-income individuals and racial minorities are actually at greatest risk,” says Wendy Troxel, a senior behavioral and social scientist at the RAND Corporation, who coauthored an analysis of socioeconomic disparities in sleep and health in the 2020 Annual Review of Public Health. Inadequate sleep among low-income adults and racial minorities contributes to higher rates of illnesses, including cardiovascular disease and dementia, both of which are more common among these groups, Troxel and her coauthors point out. One study they cite attributes more than half of the differences in health outcomes between whites and Blacks, for example, to differences in quantity or quality of sleep. You might think of this as the great sleep divide. © 2021 Annual Reviews, Inc

Keyword: Sleep; Stress
Link ID: 27881 - Posted: 06.29.2021