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

by Niko McCarty Mutations in TSC2, a gene linked to autism and a related condition called tuberous sclerosis complex, cause developing neurons to ignore chemical cues that help them connect with each other, a new study suggests. The results may explain the altered wiring patterns seen in the brains of people with such mutations. TSC2 mutations disrupt the formation of axons, the long neuronal projections that send electrical signals from one brain cell to another, past research shows. Researchers long attributed this faulty wiring to problems with mTOR, a signaling pathway that helps neurons synthesize proteins and other materials they need to grow and form connections; without TSC2, mTOR runs amok. In neurons derived from the skin of a person with tuberous sclerosis, however, the mTOR pathway is not hyperactive, the new study found. Instead, the work implicates a different signaling protein: RhoA. “We were very surprised,” says Timothy Gómez, professor of neuroscience at the University of Wisconsin-Madison, who led the new study. “We were expecting this to be all mTOR.” RhoA helps neurons reshape an internal cytoskeleton as they extend axons toward other cells. Deletions or duplications of genes in the Rho pathway are found in people with autism. Several genes in the autism-linked chromosomal region 16p11.2 also interact with RhoA. “I’m glad to see that many autism-related genes are now converging on RhoA, which actually makes a lot of sense,” says Lilia Iakoucheva, associate professor of psychiatry at the University of California, San Diego, who was not involved in the study. “The work is beautiful.” © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27880 - Posted: 06.29.2021

Kareem Clark With COVID-19 vaccines working and restrictions lifting across the country, it’s finally time for those now vaccinated who’ve been hunkered down at home to ditch the sweatpants and reemerge from their Netflix caves. But your brain may not be so eager to dive back into your former social life. Social distancing measures proved essential for slowing COVID-19’s spread worldwide – preventing upward of an estimated 500 million cases. But, while necessary, 15 months away from each other has taken a toll on people’s mental health. In a national survey last fall, 36% of adults in the U.S. – including 61% of young adults – reported feeling “serious loneliness” during the pandemic. Statistics like these suggest people would be itching to hit the social scene. But if the idea of making small talk at a crowded happy hour sounds terrifying to you, you’re not alone. Nearly half of Americans reported feeling uneasy about returning to in-person interaction regardless of vaccination status. Transparent, research-based, written by experts – and always free. So how can people be so lonely yet so nervous about refilling their social calendars? Well, the brain is remarkably adaptable. And while we can’t know exactly what our brains have gone through over the last year, neuroscientists like me have some insight into how social isolation and resocialization affect the brain.

Keyword: Stress
Link ID: 27879 - Posted: 06.29.2021

By Bruce Bower A fossil skull nicknamed “Dragon Man” has surfaced in China under mysterious circumstances, with big news for Neandertals. Dragon Man belonged to a previously unrecognized Stone Age species that replaces Neandertals as the closest known relatives of people today, researchers say. A nearly complete male skull now housed in the Geoscience Museum of Hebei GEO University in Shijiazhuang, China, represents a species dubbed Homo longi by Hebei GEO paleoanthropologist Xijun Ni and his colleagues. The scientists describe the skull, which dates to at least 146,000 years ago, and analyze its position in Homo evolution in three papers published June 25 in The Innovation. Qiang Ji, a paleontologist also at Hebei GEO, received the skull in 2018 from a farmer who said the fossil had been dug up by a coworker of his grandfather’s in 1933. During bridge construction over a river in Harbin, China, the worker allegedly scooped the skull out of river sediment. Whether or not that story is true, this fossil could help answer questions about a poorly understood period of human evolution. “The Harbin cranium presents a combination of features setting it apart from other Homo species,” Ji says. The name H. longi derives from a Chinese term for the province where it was found, which translates as “dragon river.” That term inspired the nickname Dragon Man. As in H. sapiens, the Harbin skull held a large brain situated atop a relatively short face and small cheek bones. But traits such as a long, low braincase, thick brow ridges, large molars and almost square eye sockets recall several extinct Homo populations or species, including Neandertals and H. heidelbergensis (SN: 4/1/20). © Society for Science & the Public 2000–2021

Keyword: Evolution
Link ID: 27878 - Posted: 06.26.2021

Allison Aubrey Imagine a sound that travels with you no matter where you go. Whether it's a ring, a whoosh or a crickets-like buzz, you can't escape it. "Mine was like this high-pitched sonic sound," says Elizabeth Fraser, who developed tinnitus last fall. It came on suddenly at a time when many people delayed doctor visits due to the coronavirus pandemic. "It just felt like an invasion in my head, so I was really distressed," Fraser recalls. Tinnitus is the perception of ringing when, in fact, no external sound is being produced. "You can equate it to a phantom sound," explains Sarah Sydlowski, a doctor of audiology at Cleveland Clinic. The Centers for Disease Control and Prevention estimates that 20 million Americans have chronic tinnitus. And studies show the pandemic ushered in both new cases and a worsening of the condition among people who already had it. The British Tinnitus Association reported a surge in the number of people accessing its services, including a 256% increase in the number of web chats amid the pandemic. Elizabeth Fraser started hearing a "high-pitched sonic sound" in her ears last fall. It came on suddenly at a time when many people delayed doctor visits due to the coronavirus pandemic. "It just felt like an invasion in my head, so I was really distressed," Fraser recalls. © 2021 npr

Keyword: Hearing
Link ID: 27877 - Posted: 06.26.2021

Kurt Schwenk As dinosaurs lumbered through the humid cycad forests of ancient South America 180 million years ago, primeval lizards scurried, unnoticed, beneath their feet. Perhaps to avoid being trampled by their giant kin, some of these early lizards sought refuge underground. Here they evolved long, slender bodies and reduced limbs to negotiate the narrow nooks and crevices beneath the surface. Without light, their vision faded, but to take its place, an especially acute sense of smell evolved. It was during this period that these proto-snakes evolved one of their most iconic traits – a long, flicking, forked tongue. These reptiles eventually returned to the surface, but it wasn’t until the extinction of dinosaurs many millions of years later that they diversified into myriad types of modern snakes. As an evolutionary biologist, I am fascinated by these bizarre tongues – and the role they have played in snakes’ success. Snake tongues are so peculiar they have fascinated naturalists for centuries. Aristotle believed the forked tips provided snakes a “twofold pleasure” from taste – a view mirrored centuries later by French naturalist Bernard Germain de Lacépède, who suggested the twin tips could adhere more closely to “the tasty body” of the soon-to-be snack. A 17th-century astronomer and naturalist, Giovanni Battista Hodierna, thought snakes used their tongues for “picking the dirt out of their noses … since they are always grovelling on the ground.” Others contended the tongue captured flies “with wonderful nimbleness … betwixt the forks,” or gathered air for sustenance.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 27876 - Posted: 06.26.2021

By Kim Tingley Childhood obesity has increased significantly in the United States during the past four decades. In 1980, about 5 percent of the country’s children between 2 and 19 were experiencing obesity, according to the C.D.C.; as of 2018, more than 19 percent were — and an additional 16 percent were considered overweight. Because children are far more likely to gain an unhealthful amount of weight while out of school over the summer, experts were worried last spring when in-person schooling was suspended indefinitely because of the pandemic. They feared extended closures might “exacerbate the epidemic of childhood obesity and increase disparities in obesity risk,” as researchers from the Mailman School of Public Health at Columbia University and colleagues put it in a paper in the journal Obesity in June 2020. That, in turn, would mean more children living with related conditions such as Type 2 diabetes, hypertension and fatty-liver disease. Those concerns were warranted, according to a May study in Pediatrics. Based on measurements of body mass index taken for more than 500,000 children between the ages of 2 and 17 during visits to the Children’s Hospital of Philadelphia Care Network, researchers found that, on average, between January 2019 and December 2020 the prevalence of obesity increased by almost 2 percentage points overall, from 13.7 percent to 15.4 percent. (In the most recent years for which national data is available, the increase has been 1 percentage point or less.) Black and Latino children, as well as those from families with lower incomes, displayed sharper increases than children from other groups did. Such gains early in life make it more likely that children will have higher B.M.I.s when they grow up. (Obesity already affects more than 40 percent of American adults.) “This isn’t just baby fat that’s going to go away,” says Brian Jenssen, the study’s lead author and a pediatrician at Children’s. “That’s why I think this is so alarming.” © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27875 - Posted: 06.26.2021

by Rachel Zamzow Most mornings, Huda Zoghbi, 67, climbs a glass-encased, curling staircase to reach her lab on the top and 13th floor of the Jan and Dan Duncan Neurological Research Institute in Houston, Texas. The twisting glass tower, which she designed with a team of architects, echoes the double helix of DNA — a structure that has been central to her career-long quest to uncover genes underlying neurological conditions. As the institute’s director — and as a scientist— she is known for going beyond the standard job description. Genetics researchers often cast a wide net and sequence thousands of genes at a time. But in her prolific career, Zoghbi has focused on a handful of genes, methodically building up an understanding of their function one careful step at a time. Thanks to that approach, Zoghbi has made a number of landmark discoveries, including identifying the genetic roots of Rett syndrome, an autism-related condition that primarily affects girls, as well as the genetic mutations that spur spinocerebellar ataxia, a degenerative motor condition. She has authored more than 350 journal articles. Her accomplishments have earned her almost every major biology and neuroscience research award, including the prestigious Breakthrough Prize in 2017 and the Brain Prize in 2020. “She’s clearly the international leader in the field,” said the late Stephen Warren, professor of human genetics at Emory University in Atlanta, Georgia. Zoghbi never set out to lead a large research center, she says — her heart is in the lab. That said, she has excelled at it: Since the institute’s inception in 2010, it has grown to host more than 200 scientists and fostered more than 70 new disease gene discoveries. © 2021 Simons Foundation

Keyword: Movement Disorders; Development of the Brain
Link ID: 27874 - Posted: 06.26.2021

As I lean back in the leather recliner, my limbs feel heavy. The strong dose of ketamine I've just taken is making it harder to move, so I struggle to put on my headphones and eyeshades. Soothing music lulls me into deep relaxation, as my consciousness starts to float away from my body and into a world of swirling lights, colours and images. I'm not at a new-age music festival, or in a seedy underground drug den. This fully-legal experience is taking place under medical supervision at Field Trip Health in Toronto, a clinic that offers psychedelic-assisted therapy for those suffering treatment-resistant mental illnesses like depression and PTSD. The clinic, which was the first of its kind in Canada, opened last year. Since then, similar clinics have opened in Quebec, Alberta, Saskatchewan, B.C., and Nova Scotia. Ketamine was first approved for use in Canada and the U.S. as a general anesthetic more than 50 years ago. Since then it has gained a reputation as a party drug, with names like Special K or Vitamin K. Today, it's increasingly being used as a fast-acting and effective treatment for depression. But it isn't without controversy. I've dealt with bouts of depression and suicidal thoughts for about as long as I can remember. By the fall of 2020, after months of isolation due to the COVID-19 pandemic had taken their toll, my depression was as bad as it had ever been. ©2021 CBC/Radio-Canada.

Keyword: Depression; Drug Abuse
Link ID: 27873 - Posted: 06.26.2021