By Kashmir Hill and Jeremy White There are now businesses that sell fake people. On the website Generated.Photos, you can buy a “unique, worry-free” fake person for $2.99, or 1,000 people for $1,000. If you just need a couple of fake people — for characters in a video game, or to make your company website appear more diverse — you can get their photos for free on ThisPersonDoesNotExist.com. Adjust their likeness as needed; make them old or young or the ethnicity of your choosing. If you want your fake person animated, a company called Rosebud.AI can do that and can even make them talk. These simulated people are starting to show up around the internet, used as masks by real people with nefarious intent: spies who don an attractive face in an effort to infiltrate the intelligence community; right-wing propagandists who hide behind fake profiles, photo and all; online harassers who troll their targets with a friendly visage. The A.I. system sees each face as a complex mathematical figure, a range of values that can be shifted. Choosing different values — like those that determine the size and shape of eyes — can alter the whole image. For other qualities, our system used a different approach. Instead of shifting values that determine specific parts of the image, the system first generated two images to establish starting and end points for all of the values, and then created images in between. The creation of these types of fake images only became possible in recent years thanks to a new type of artificial intelligence called a generative adversarial network. In essence, you feed a computer program a bunch of photos of real people. It studies them and tries to come up with its own photos of people, while another part of the system tries to detect which of those photos are fake. The back-and-forth makes the end product ever more indistinguishable from the real thing. The portraits in this story were created by The Times using GAN software that was made publicly available by the computer graphics company Nvidia. © 2020 The New York Times Company

Keyword: Attention
Link ID: 27589 - Posted: 11.21.2020

Researchers at the National Eye Institute (NEI) have decoded brain maps of human color perception. The findings, published today in Current Biology, open a window into how color processing is organized in the brain, and how the brain recognizes and groups colors in the environment. The study may have implications for the development of machine-brain interfaces for visual prosthetics. NEI is part of the National Institutes of Health. “This is one of the first studies to determine what color a person is seeing based on direct measurements of brain activity,” said Bevil Conway, Ph.D., chief of NEI’s Unit on Sensation, Cognition and Action, who led the study. “The approach lets us get at fundamental questions of how we perceive, categorize, and understand color.” The brain uses light signals detected by the retina’s cone photoreceptors as the building blocks for color perception. Three types of cone photoreceptors detect light over a range of wavelengths. The brain mixes and categorizes these signals to perceive color in a process that is not well understood. To examine this process, Isabelle Rosenthal, Katherine Hermann, and Shridhar Singh, post-baccalaureate fellows in Conway’s lab and co-first authors on the study, used magnetoencephalography or “MEG,” a 50-year-old technology that noninvasively records the tiny magnetic fields that accompany brain activity. The technique provides a direct measurement of brain cell activity using an array of sensors around the head. It reveals the millisecond-by-millisecond changes that happen in the brain to enable vision. The researchers recorded patterns of activity as volunteers viewed specially designed color images and reported the colors they saw.

Keyword: Vision; Brain imaging
Link ID: 27588 - Posted: 11.21.2020

By Lisa Sanders, M.D. It started to drizzle just moments after the 24-year-old man crossed the finish line of the 2017 New York City Marathon. It was his first marathon, and he felt both elated and exhausted as the medal given for completing the brutal race was draped around his neck. A goody bag containing an energy drink was put in his left hand. It felt strangely heavy. His whole body ached and trembled with fatigue, but somehow that left arm felt even more tired. Unconcerned, he switched the bag to his right hand and went in search of his partner. Recovery took longer than he expected. It was a day and a half before his legs were strong enough for him to walk down stairs facing forward, rather than the sideways shuffle that his tired muscles insisted on. But by the end of the week he felt mostly normal. Only that left shoulder remained tired, sore and stiff. He went to a nearby walk-in clinic just south of City Hall. The nurse practitioner who examined him thought he had a rotator-cuff injury. She recommended a nonsteroidal anti-inflammatory like ibuprofen, physical therapy and time. The ibuprofen didn’t help much; neither did the physical therapy. That weekend he headed to the gym — his first workout since the race. He did his usual set of reps on his right biceps and triceps. But when he transferred the 25-pound dumbbell to his left hand, it seemed heavier. He struggled through two curls, but on the third the muscles in his arm turned wobbly. He grabbed the weight with his right hand and lowered it to the ground. By the time he got home, straightening his aching arm was excruciating, as if the muscles were too short to allow a full extension. That scared him. And it only got worse. The next day his whole arm was achy and tight. He couldn’t even work on his computer. Thinking back, the young runner questioned the assumption — shared by both him and the nurse practitioner — that the injury had occurred during the race. Now he suspected it started weeks earlier. © 2020 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27587 - Posted: 11.21.2020

Diana Kwon It all began with a cough. Three years ago Tracey McNiven, a Scottish woman in her mid-30s, caught a bad chest infection that left her with a persistent cough that refused to subside, even after medication. A few months later strange symptoms started to appear. McNiven noticed numbness spreading through her legs and began to feel that their movement was out of her control. When she walked, she felt like a marionette, with someone else pulling the strings. Over the course of two weeks the odd loss of sensation progressively worsened. Then, one evening at home, McNiven's legs collapsed beneath her. “I was lying there, and I felt like I couldn't breathe,” she recalls. “I couldn't feel below my waist.” McNiven's mother rushed her to the hospital where she remained for more than half a year. During her first few weeks in the hospital, McNiven endured a barrage of tests as doctors tried to uncover the cause of her symptoms. It could be a progressive neurodegenerative condition such as motor neuron disease, they thought. Or maybe it was multiple sclerosis, a disease in which the body's own immune cells attack the nervous system. Bafflingly, however, the brain scans, blood tests, spinal taps and everything else came back normal. McNiven's predicament is not uncommon. According to one of the most comprehensive assessments of neurology clinics to date, roughly a third of patients have neurological symptoms that are deemed to be either partially or entirely unexplained. These may include tremor, seizures, blindness, deafness, pain, paralysis and coma and can parallel those of almost any neurological disease. In some patients, such complications can persist for years or even decades; some people require wheelchairs or cannot get out of bed. Although women are more often diagnosed than men, such seemingly inexplicable illness can be found in anyone and across the life span. © 2020 Scientific American

Keyword: Attention; Emotions
Link ID: 27586 - Posted: 11.18.2020

Jon Hamilton During deep sleep, the brain appears to wash away waste products that increase the risk for Alzheimer's disease. A host of new research studies suggest that this stage of sleep — when dreams are rare and the brain follows a slow, steady beat – can help reduce levels of beta-amyloid and tau, two hallmarks of the disease. "There is something about this deep sleep that is helping protect you," says Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley. The research comes after decades of observations linking poor sleep to long-term problems with memory and thinking, Walker says. "We are now learning that there is a significant relationship between sleep and dementia, particularly Alzheimer's disease." The strongest evidence involves deep sleep, he says. That's when body temperature drops and the brain begins to produce slow, rhythmic electrical waves. So Walker and a team of scientists set out to answer a question: "Can I look into your future and can I accurately estimate how much beta-amyloid you're going to accumulate over the next two years, the next four years, the next six years, simply on the basis of your sleep tonight?" To find out, Walker's team studied 32 people in their 70s who had taken part in a sleep study that looked for the slow electrical waves that signal deep sleep. None of the participants had memory problems. the brain cells of people with Alzheimer's. © 2020 npr

Keyword: Sleep; Alzheimers
Link ID: 27585 - Posted: 11.18.2020

By Jessica Wapner We are living through an inarguably challenging time. The U.S. has been facing its highest daily COVID-19 case counts yet. Uncertainty and division continue to dog the aftermath of the presidential election. And we are heading into a long, cold winter, when socializing outdoors will be less of an option. We are a nation and a world under stress. But Andrew Huberman, a neuroscientist at Stanford University who studies the visual system, sees matters a bit differently. Stress, he says, is not just about the content of what we are reading or the images we are seeing. It is about how our eyes and breathing change in response to the world and the cascades of events that follow. And both of these bodily processes also offer us easy and accessible releases from stress. Huberman’s assertions are based on both established and emerging science. He has spent the past 20 years unraveling the inner workings of the visual system. In 2018, for example, his lab reported its discovery of brain pathways connected with fear and paralysis that respond specifically to visual threats. And a small but growing body of research makes the case that altering our breathing can alter our brain. In 2017 Mark Krasnow of Stanford University, Jack Feldman of the University of California, Los Angeles, and their colleagues identified a tight link between neurons responsible for controlling breathing and the region of the brain responsible for arousal and panic. This growing understanding of how vision and breathing directly affect the brain—rather than the more nebulous categories of the mind and feelings—can come in handy as we continue to face mounting challenges around the globe, across the U.S. and in our own lives. Scientific American spoke with Huberman about how it all works. © 2020 Scientific American

Keyword: Stress; Vision
Link ID: 27584 - Posted: 11.18.2020

Terry Gross Food science writer Harold McGee was in the middle of writing Nose Dive, his book about the science of smell, when he woke up one morning and realized that he couldn't smell his own coffee. Loss of smell has since become associated with COVID-19. In McGee's case, it was the byproduct of a sinus infection. McGee remembers feeling panicked. "I have friends in the kind of clinical side of taste and smell research. And so I immediately contacted them to find out what I could do and why this had happened," he says. "And they basically said, 'You're going to have to wait and see.' " Over the course of a few months, McGee's sense of smell gradually returned. But he still remembers what it was like to live in an odorless world. "It's the kind of thing where you don't notice something until it's gone," he says. "I spent less and less time cooking. There was no point in going out to restaurants because I wasn't really going to enjoy it." McGee's new book is about how smell is essential to our sense of taste, why things smell the way they do and the ways different chemicals combine to create surprising (and sometimes distasteful) odors. "One of the great pleasures of delving into smells in general was discovering over and over again that things that we enjoy in foods are actually found elsewhere in the world," he says. "And in as unlikely places as cat pee and human sweat, for example." © 2020 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27583 - Posted: 11.16.2020

Linda Geddes Many of the side-effects attributed to statins could be down to the “nocebo effect”, which occurs when someone expects to experience negative symptoms – even if the drug is a placebo – a study suggests. Statins are one of the most widely prescribed drugs in the UK, taken by nearly eight million people to reduce their risk of cardiovascular disease by lowering cholesterol levels. Yet, despite their effectiveness, up to a fifth of people stop taking them because of side-effects, such as fatigue, muscle aches, joint pain and nausea. Clinical studies have suggested, however, the incidence of side-effects is far lower. Researchers led by Frances Wood and Dr James Howard at Imperial College London recruited 60 patients who had been on statins, but stopped taking them owing to adverse effects. They were persuaded to resume treatment, and given four bottles containing atorvastatin, four bottles containing identical-looking placebo pills and four empty bottles, to be taken in a randomly prescribed order over the course of a year – including four months taking no pills. Each day, they recorded any side-effects on a smartphone, ranking their intensity from zero to 100. The researchers found 90% of symptoms experienced by the patients were present when they took placebo tablets. Also, 24 patients stopped taking tablets for at least one month of the trial, citing intolerable side-effects – amounting to 71 stoppages in total. Of these, 31 occurred during placebo months and 40 were during statin months. The results were published in the New England Journal of Medicine. © 2020 Guardian News & Media Limited

Keyword: Pain & Touch; Attention
Link ID: 27582 - Posted: 11.16.2020

By Catherine Zuckerman It’s 3 a.m. and you’ve been struggling for hours to fall asleep. Morning draws nearer and your anxiety about being exhausted the next day intensifies — yet again. If this sounds familiar, you’re not alone. Among the many disruptions of 2020, insomnia may rank high on the list. Data on how the pandemic has affected sleep is limited because biomedical research can take years to shake out and most studies to date have been small. But evidence from China and Europe suggests that prolonged confinement is altering sleep in adults as well as children. Doctors in the United States are seeing it too. “I think Covid and the election have affected sleep and could be considered a kind of trauma,” said Nancy Foldvary-Schaefer, director of the Cleveland Clinic Sleep Disorders Center. “A lot of people that I talk to — patients and non-patients and colleagues and family — have more anxiety generally now probably because of these two stressors, and high anxiety is clearly associated with insomnia.” Whether you’re suddenly tossing and turning at bedtime or waking up in the middle of the night, the first step toward better sleep is to figure out what’s triggering your insomnia. Once you do that, you can take action to prevent it from becoming chronic — a clinical sleep disorder that should be treated by a sleep-medicine specialist. Stressful and upsetting experiences like the death of a loved one or the loss of a job — two widespread realities of Covid-19 — are known psychological triggers for insomnia. If your insomnia is tied to such an event, the quickest way to get help is to call your doctor. One thing many doctors suggest is cognitive behavioral therapy, or C.B.T. C.B.T., or C.B.T.-I. for insomnia, is a standard treatment for both acute and chronic insomnia and includes a variety of techniques. Meditation, mindfulness and muscle relaxation can help people whose sleep problems are tied to a stressful event. C.B.T. for insomnia typically lasts from six to eight weeks and “works in about two-thirds to three-quarters of patients,” said Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles, David Geffen School of Medicine. © 2020 The New York Times Company

Keyword: Sleep; Stress
Link ID: 27581 - Posted: 11.16.2020

By Elisabeth Egan Two years ago, Michael J. Fox had surgery to remove a benign tumor on his spinal cord. The actor and activist, who had been living with Parkinson’s disease for nearly three decades, had to learn to walk all over again. Four months later, he fell in the kitchen of his Upper East Side home and fractured his arm so badly that it had to be stabilized with 19 pins and a plate. Mired in grueling, back-to-back recoveries, he started to wonder if he had oversold the idea of hope in his first three memoirs, “Lucky Man,” “Always Looking Up” and “A Funny Thing Happened on the Way to the Future.” “I had this kind of crisis of conscience,” Fox said during a video interview last month from his Manhattan office, where pictures of Tracy Pollan, his wife of 31 years, and his dog, Gus, hung behind him. “I thought, what have I been telling people? I tell people it’s all going to be OK — and it might suck!” His solution was to channel that honesty into a fourth memoir, “No Time Like the Future,” which Flatiron is publishing on Nov. 17. For an example of his new outlook, consider his perspective on traveling by wheelchair. “It can be a frustrating and isolating experience, allowing someone else to determine the direction I’m going and the rate of speed I can travel. The pusher is in charge,” Fox writes. “From the point of view of the occupant of the chair, it’s a world of asses and elbows. No one can hear me. To compensate, I raise my voice and suddenly feel like Joan Crawford in ‘What Ever Happened to Baby Jane?,’ barking out orders.” He continues: “Generally the person in control is a stranger, an airport or hotel employee. I’m sure that if we could look each other in the eye, we’d recognize our mutual humanity. But often in the wheelchair, I’m luggage. I’m not expected to say much. Just sit still.” Later, he adds, “No one listens to luggage.” Before the spinal surgery, Fox was working on a book about golf. “Then life happened,” he said. “I started thinking about what it meant to be able to move and express myself physically, to have that taken away. And then dealing with the surrender it takes to lie down and say, ‘Cut me open.’ I don’t know what that’s like for anybody else, but I can figure out what it’s like for me and write it down.” © 2020 The New York Times Company

Keyword: Parkinsons
Link ID: 27580 - Posted: 11.14.2020

Joel Frohlich Three years ago, I asked, “What the heck is a claustrum?” In that post, I described the mystery of this oddly shaped brain region, located just below the cerebral cortex. Because the claustrum is vanishingly thin in its cross section (think of a pancake shaped like North America), very few patients or lab animals have experienced lesions that specifically destroy the claustrum. For this reason, it’s difficult to pin down what happens when just this brain region (and not others) goes offline. But given its wealth of connections to other brain areas, neuroscientist Christof Koch speculated in 2017 that “the claustrum could be coordinating inputs and outputs across the brain to create consciousness.” This idea is supported by a report of a woman with epilepsy who lost consciousness after her claustrum was electrically stimulated, and perhaps also by the consciousness-transforming effects of Salvinorin A, a drug that binds to receptors that are abundant in the claustrum and alters body image. Could the claustrum, an enigma of the brain, also be the key to the conscious mind? Well, now we have the answer. Using a genetic engineering technique called optogenetics that enables neurons to fire impulses in response to blue light, a team at the RIKEN Brain Science Institute in Japan has discovered what the heck the claustrum actually does. During deep sleep when you’re not dreaming, your cerebral cortex shows slow waves of electrical activity. These waves are very synchronous, meaning they reflect the coordinated activity of many neurons, more so than the smaller, faster waves that are generally present when you are either awake or dreaming. How does the brain coordinate the activity of so many neurons? It turns out that the claustrum plays a key role. © 2020 Sussex Publishers, LLC

Keyword: Consciousness
Link ID: 27579 - Posted: 11.14.2020

By Cheryl Maguire When my 15-year-old son was given a diagnosis of attention deficit hyperactivity disorder at age 7, I was told that it was a lifelong chronic condition. So I felt a little bit hopeful when a study published last winter in the Journal of Developmental and Behavioral Pediatrics said that “an estimated 30 percent to 60 percent of children diagnosed with A.D.H.D. no longer meet diagnostic criteria for this disorder by late adolescence.” Does that mean they outgrew it? There is no simple answer, said Thomas Power, director of the center for management of A.D.H.D. at Children’s Hospital of Philadelphia, and the senior author of the study. He was one of eight experts I consulted, and while they fell into different camps on whether someone can outgrow A.D.H.D., they all agreed that the answer is complicated. Some said there could be a genetic component to outgrowing A.D.H.D., while others told me that certain coping skills and job choices play a prominent role in lessening symptoms, which could make it seem that the person no longer has it. Russell Barkley, a clinical professor of psychiatry at the Virginia Commonwealth University Medical Center, clarified that ceasing to meet the definition of A.D.H.D. in the Diagnostic and Statistical Manual of Mental Disorders, the main resource that clinicians use to make a diagnosis, does not mean that the person no longer has the issues of A.D.H.D. “People are outgrowing the D.S.M. criteria but not outgrowing their disorder for the most part,” Dr. Barkley said. “Diagnosing A.D.H.D. is not like leukemia, where you do a blood test and you know definitively you have leukemia,” said Dr. William Barbaresi, a developmental behavioral pediatrician at Children’s Hospital in Boston, and professor of pediatrics at Harvard Medical School. When a young child is given an A.D.H.D. diagnosis, doctors and clinicians rely on patient, parent and teacher feedback. But when a late adolescent or adult is assessed, it is normally based on self-reports only. “There are a lot of reasons to wonder how accurate that report is since it is difficult to evaluate yourself,” said Dr. Barbaresi. And Dr. Power noted, “Individuals with A.D.H.D. tend to underreport their symptoms.” © 2020 The New York Times Company

Keyword: ADHD
Link ID: 27578 - Posted: 11.14.2020

In a 2009 TED Talk, Israeli neuroscientist Henry Markram made a shocking claim: he was going to create a machine version of human brain within 10 years. The project was catnip to filmmaker Noah Hutton, who began documenting Markram's quest. Ultimately, Hutton followed Markram for a decade — but the scientist's lofty goal remains conspicuously incomplete. The resulting film, In Silico, finally makes its world premiere as part of the online version of the DOC NYC film festival on November 11. The film traces Markram’s journey with the Human Brain Project, from the project’s inception to its $1.4 billion in funding from the European Commission — and how it failed to meet its 10-year goal by 2019. Following a neuroscientist for a decade reveals a lot of highs and lows. Hutton presents the controversies by interviewing both the Human Brain Project team and its critics, including Princeton neuroscientist Sebastian Seung, researcher Zach Mainen at the Champalimaud Centre for the Unknown based in Portugal, and experimental cognitive psychologist Stanislas Dehane, who is professor at Collège de France in Paris. The film also features candid interviews with neuroscientists Christof Koch, who head's up the Allen Institute's MindScope Program, Harvard University's Jeremy R. Knowles Professor of Molecular and Cellular Biology Jeff W. Lichtman, and Stanford University neuroscience adjunct professor David Eagleman. Neuroscientists Idan Segev of Hebrew University in Israel, Cori Bargmann, Torsten N. Weisel Professor of Genetics and Genomics and Neuroscience and Behavior at Rockefeller University, and Cold Spring Harbor Lab professor Anne Churchland.

Keyword: Brain imaging
Link ID: 27577 - Posted: 11.14.2020

By Benedict Carey Merriam-Webster’s defines a time warp as a “discontinuity, suspension or anomaly” in the otherwise normal passage of time; this year all three terms could apply. It seems like March happened 10 years ago; everyday may as well be Wednesday, and still, somehow, here come the holidays — fast, just like every year. Some bard or novelist may yet come forth to help explain the paradoxes of pandemic time, both its Groundhog Days and the blurs of stress and fear for those on the front lines, or who had infectious people in their household. But brain science also has something to say about the relationship between perceived time and the Greenwich Mean variety, and why the two may slip out of sync. In a new study, a research team based in Dallas reported the first strong evidence to date of so-called “time cells” in the human brain. The finding, posted by the journal PNAS, was not unexpected: In recent years, several research groups have isolated neurons in rodents that track time intervals. It’s where the scientists look for these cells, and how they identified them, that provide some insight into the subjective experiences of time. “The first thing to say is that, strictly speaking, there is no such thing as ‘time cells’ in the brain,” said Gyorgy Buzsaki, a neuroscientist at New York University who was not involved in the new research. “There is no neural clock. What happens in the brain is neurons change in response to other neurons.” He added, “Having said that, it’s a useful concept to talk about how this neural substrate represents the passage of what we call time.” In the new study, a team led by Dr. Bradley Lega, a neurosurgeon at UT Southwestern Medical Center, analyzed the firing of cells in the medial temporal area, a region deep in the brain that is essential for memory formation and retrieval. It’s a natural place to look: Memories must be somehow “time-stamped” to retain some semblance of sequence, or chronological order. © 2020 The New York Times Company

Keyword: Attention
Link ID: 27576 - Posted: 11.10.2020

by Angie Voyles Askham Editing DNA in embryonic and newborn mice by using CRISPR technology can override mutations underlying Angelman syndrome and prevent many of the condition’s traits, according to a new study1. The effects last for at least 17 months and may be permanent, the researchers say. “It’s very exciting,” says Steven Kushner, professor of psychiatry at Columbia University, who was not involved in the study. Angelman syndrome usually stems from a mutation in or deletion of the UBE3A gene. People have two copies of the gene — one from each parent — but typically only the one passed down from the mother is active in neurons. Mutations that stymie that copy can lead to a lack of UBE3A protein in the brain, causing the syndrome’s core traits: developmental delays, motor dysfunction, speech impairments, seizures and, often, autism. These traits improve in response to treatments that activate the silent yet intact paternal copy of UBE3A and boost production of the protein in Angelman syndrome model mice2,3. But these treatments wear off over time, requiring repeated injections into the spinal fluid or brain. The new therapy is effective after only two doses, says lead researcher Mark Zylka, professor of cell biology and physiology at the University of North Carolina at Chapel Hill. The strategy uses the enzyme CRISPR-Cas9 to cut and edit DNA encoding an ‘antisense RNA’ molecule that ordinarily serves to block production of UBE3A protein from the paternal copy of the gene. The technique also rouses the silent paternal copy of the gene in cultured human neurons, suggesting that it might work in people. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27575 - Posted: 11.10.2020

By James Gorman Dogs go through stages in their life, just as people do, as is obvious to anyone who has watched their stiff-legged, white-muzzled companion rouse themselves to go for one more walk. Poets from Homer to Pablo Neruda have taken notice. As have folk singers and story tellers. Now science is taking a turn, in the hope that research on how dogs grow and age will help us understand how humans age. And, like the poets before them, scientists are finding parallels between the two species. Their research so far shows that dogs are similar to us in important ways, like how they act during adolescence and old age, and what happens in their DNA as they get older. They may be what scientists call a “model” for human aging, a species that we can study to learn more about how we age and perhaps how to age better. Most recently, researchers in Vienna have found that dogs’ personalities change over time. They seem to mellow in the same way that most humans do. The most intriguing part of this study is that like people, some dogs are just born old, which is to say, relatively steady and mature, the kind of pup that just seems ready for a Mr. Rogers cardigan. “That’s professor Spot, to you, thank you, and could we be a little neater when we pour kibble into my dish?” Mind you, the Vienna study dogs were all Border collies, so I’m a little surprised that any of them were mature. That would suggest a certain calm, a willingness to tilt the head and muse that doesn’t seem to fit the breed, with its desperate desire to be constantly chasing sheep, geese, children or Frisbees. Another recent paper came to the disturbing conclusion that the calculus of seven dog years for every human year isn’t accurate. To calculate dog years, you must now multiply the natural logarithm of a dog’s age in human years by 16 and then add 31. Is that clear? It’s actually not as hard as it sounds, as long as you have a calculator or internet access. For example the natural log of 6 is 1.8, roughly, which, multiplied by 16 is about 29, which, plus 31, is 60. OK, it’s not that easy, even with the internet. © 2020 The New York Times Company

Keyword: Development of the Brain; Evolution
Link ID: 27574 - Posted: 11.10.2020

By Linda Searing The “baby blues” that women can experience after giving birth usually go away within a week or two, but it now appears that more severe depressive symptoms, known as postpartum depression, may affect some new mothers for at least three years. Research from the National Institutes of Health, which tracked 4,866 women for three years after childbirth, found that about 25 percent of the women reported moderate to high levels of depressive symptoms at some point and that the remaining 75 percent experienced low-level depressive symptoms throughout the study. The “baby blues” typically include such symptoms as mood swings, anxiety and trouble sleeping, whereas postpartum depression symptoms — generally more intense and longer lasting — may include excessive crying, overwhelming fatigue, loss of appetite, difficulty bonding with the baby, feelings of inadequacy, hopelessness and more. The NIH research, published in the journal Pediatrics, encourages pediatricians to screen their tiny patients’ mothers for depressive symptoms during the children’s regular checkups, noting that “mothers’ mental health is critical to children’s well-being and development.” The researchers note that maternal depression increases a child’s risk for cognitive, emotional and behavioral problems. Getting treatment, however, should not only ease a mother’s symptoms but also improve her child’s odds for a favorable developmental outcome.

Keyword: Depression; Development of the Brain
Link ID: 27573 - Posted: 11.10.2020

By Giorgia Guglielmi, Spectrum A small clinical trial of a gene therapy for Angelman syndrome—a rare genetic condition related to autism—is on hold after two participants temporarily lost the ability to walk. The safety issue is important to resolve, experts say, given that the therapy otherwise appears to be effective, and the trial could guide treatment strategies for similar brain conditions. Biopharmaceutical company Ultragenyx in Novato, California, in collaboration with Florida-based biotech startup GeneTx, launched the trial in February to assess the safety of a therapy for Angelman syndrome, a neurodevelopmental condition characterized by intellectual disability, balance and motor problems, seizures, sleep problems and, in some cases, autism. Angelman syndrome results from the mutation or absence of a gene called UBE3A. People inherit two copies of UBE3A. Typically, only the maternal copy is active in neurons and the paternal copy is silent. But in people with Angelman syndrome, the maternal copy is mutated or missing, so their brain cells express no active UBE3A protein. The drug developed by Ultragenyx and GeneTx, called GTX-102, is a short snippet of RNA called an antisense oligonucleotide that activates the paternal copy of UBE3A and aims to restore the protein to typical levels. Three other companies—Roche, Biogen, and Ionis—are pursuing similar therapies for the syndrome. On 26 October, Ultragenyx and GeneTx reported that the clinical trial had enrolled five individuals with Angelman syndrome, aged 5 to 15. The plan had been to administer to each participant a dose of GTX-102 once a month over four months. Researchers injected the drug directly into the nutrient-rich solution that envelops the brain and spinal cord through a site in the lower back. © 2020 American Association for the Advancement of Science

Keyword: Autism
Link ID: 27572 - Posted: 11.07.2020

Alison Abbott Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ. The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. Norins wanted to reward work that would make the infection idea more persuasive. The amyloid hypothesis has become “the one acceptable and supportable belief of the Established Church of Conventional Wisdom”, says Norins. “The few pioneers who did look at microbes and published papers were ridiculed or ignored.” In large part, this was because some early proponents of the infection theory saw it as a replacement for the amyloid hypothesis. But some recent research has provided intriguing hints that the two ideas could fit together — that infection could seed some cases of Alzheimer’s disease by triggering the production of amyloid clumps. The data hint at a radical role for amyloid in neurons. Instead of just being a toxic waste product, amyloid might have an important job of its own: helping to protect the brain from infection. But age or genetics can interrupt the checks and balances in the system, turning amyloid from defender into villain. And that idea suggests new avenues to explore for potential therapies. To test the theory further, scientists are now developing animal models that mimic Alzheimer’s disease more closely. “We are taking the ideas seriously,” says neuroscientist Bart de Strooper, director of the UK Dementia Research Institute at University College London. © 2020 Springer Nature Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 27571 - Posted: 11.07.2020

By Laura Sanders The fate of a potential new Alzheimer’s drug is still uncertain. Evidence that the drug works isn’t convincing enough for it to be approved, outside experts told the U.S. Food and Drug Administration during a Nov. 6 virtual meeting that at times became contentious. The scientists and clinicians were convened at the request of the FDA to review the evidence for aducanumab, a drug that targets a protein called amyloid-beta that accumulates in the brains of people with Alzheimer’s. The drug is designed to stick to A-beta and stop it from forming larger, more dangerous clumps. That could slow the disease’s progression but not stop or reverse it. When asked whether a key clinical study provided strong evidence that the drug effectively treated Alzheimer’s, eight of 11 experts voted no. One expert voted yes, and two were uncertain. The FDA is not bound to follow the recommendations of the guidance committee, though it has historically done so. If ultimately approved, the drug would be a milestone, says neurologist and neuroscientist Arjun Masurkar of New York University Langone’s Alzheimer’s Disease Research Center. Aducanumab “would be the first therapy that actually targets the underlying disease itself and slows progression.” Developed by the pharmaceutical company Biogen, which is based in Cambridge, Mass., the drug is controversial. That’s because two large clinical trials of aducanumab have yielded different outcomes, one positive and one negative (SN: 12/5/19). The trials were also paused at one point, based on analyses that suggested the drug didn’t work. © Society for Science & the Public 2000–2020.

Keyword: Alzheimers
Link ID: 27570 - Posted: 11.07.2020