By Christof Koch Consider the following experiences: • You're headed toward a storm that's a couple of miles away, and you've got to get across a hill. You ask yourself: “How am I going to get over that, through that?” • You see little white dots on a black background, as if looking up at the stars at night. Advertisement • You look down at yourself lying in bed from above but see only your legs and lower trunk. These may seem like idiosyncratic events drawn from the vast universe of perceptions, sensations, memories, thoughts and dreams that make up our daily stream of consciousness. In fact, each one was evoked by directly stimulating the brain with an electrode. As American poet Walt Whitman intuited in his poem “I Sing the Body Electric,” these anecdotes illustrate the intimate relationship between the body and its animating soul. The brain and the conscious mind are as inexorably linked as the two sides of a coin. Recent clinical studies have uncovered some of the laws and regularities of conscious activity, findings that have occasionally proved to be paradoxical. They show that brain areas involved in conscious perception have little to do with thinking, planning and other higher cognitive functions. Neuroengineers are now working to turn these insights into technologies to replace lost cognitive function and, in the more distant future, to enhance sensory, cognitive or memory capacities. For example, a recent brain-machine interface provides completely blind people with limited abilities to perceive light. These tools, however, also reveal the difficulties of fully restoring sight or hearing. They underline even more the snags that stand in the way of sci-fi-like enhancements that would enable access to the brain as if it were a computer storage drive. © 2021 Scientific American,

Keyword: Consciousness
Link ID: 27865 - Posted: 06.19.2021

By Christa Lesté-Lasserre In the animal kingdom, killer whales are social stars: They travel in extended, varied family groups, care for grandchildren after menopause, and even imitate human speech. Now, marine biologists are adding one more behavior to the list: forming fast friendships. A new study suggests the whales rival chimpanzees, macaques, and even humans when it comes to the kinds of “social touching” that indicates strong bonds. The study marks “a very important contribution to the field” of social behavior in dolphins and whales, says José Zamorano-Abramson, a comparative psychologist at the Complutense University of Madrid who wasn’t involved in the work. “These new images show lots of touching of many different types, probably related to different kinds of emotions, much like the complex social dynamics we see in great apes.” Audio and video recordings have shown how some marine mammals maintain social structures—including male dolphins that learn the “names” of close allies. But there is little footage of wild killer whales—which hunt and play in open water. Although the whales only swim at about 6 kilometers per hour, it’s hard to fully observe them from boats, and they might not act naturally near humans, Zamorano-Abramson says. That’s where drone technology came swooping in. Michael Weiss, a behavioral ecologist at the Center for Whale Research in Friday Harbor, Washington, teamed up with colleagues to launch unmanned drones from their 6.5-meter motorboat and from the shores of the northern Pacific Ocean, flying them 30 to 120 meters above a pod of 22 southern resident killer whales. That was high enough to respect federal aviation requirements—and not bother the whales. They logged 10 hours of footage over a 10-day period, marking the first time drones have been used to study friendly physical contacts in any cetacean. © 2021 American Association for the Advancement of Science.

Keyword: Evolution; Stress
Link ID: 27864 - Posted: 06.19.2021

By Diana Kwon Long before the earliest animals swam through the water-covered surface of Earth’s ancient past, one of the most important encounters in the history of life took place. A primitive bacterium was engulfed by our oldest ancestor — a solo, free-floating cell. The two fused to form a mutually beneficial relationship that has lasted more than a billion years, with the latter providing a safe, comfortable home and the former becoming a powerhouse, fueling the processes necessary to maintain life. That’s the best hypothesis to date for how the cellular components, or organelles, known as mitochondria came to be. Today, trillions of these bacterial descendants live within our bodies, churning out ATP, the molecular energy source that sustains our cells. Despite being inextricably integrated into the machinery of the human body, mitochondria also carry remnants of their bacterial past, such as their own set of DNA. The DNA that constitutes the human genome is contained within the nucleus of our cells. But mitochondria possess their own set of circular DNA, which is likely a remnant of their ancient bacterial past. These features make mitochondria both a critical element of our cells and a potential source of problems. Like the DNA inside the nuclei of our cells that makes up the human genome, mitochondrial DNA can harbor mutations. Age, stress and other factors may disrupt mitochondria’s many functions. On top of that, mitochondrial injury can release molecules that, due to their similarities to those made by bacteria, can be mistaken by our immune system as foreign invaders, triggering a harmful inflammatory response against our own cells. © 2021 Annual Reviews, Inc

Keyword: Schizophrenia; Alzheimers
Link ID: 27863 - Posted: 06.19.2021

Christopher M. Filley One of the most enduring themes in human neuroscience is the association of higher brain functions with gray matter. In particular, the cerebral cortex—the gray matter of the brain's surface—has been the primary focus of decades of work aiming to understand the neurobiological basis of cognition and emotion. Yet, the cerebral cortex is only a few millimeters thick, so the relative neglect of the rest of the brain below the cortex has prompted the term “corticocentric myopia” (1). Other regions relevant to behavior include the deep gray matter of the basal ganglia and thalamus, the brainstem and cerebellum, and the white matter that interconnects all of these structures. On page 1304 of this issue, Zhao et al. (2) present compelling evidence for the importance of white matter by demonstrating genetic influences on structural connectivity that invoke a host of provocative clinical implications. Insight into the importance of white matter in human behavior begins with its anatomy (3–5) (see the figure). White matter occupies about half of the adult human brain, and some 135,000 km of myelinated axons course through a wide array of tracts to link gray matter regions into distributed neural networks that serve cognitive and emotional functions (3). The human brain is particularly well interconnected because white matter has expanded more in evolution than gray matter, which has endowed the brain of Homo sapiens with extensive structural connectivity (6). The myelin sheath, white matter's characteristic feature, appeared late in vertebrate evolution and greatly increased axonal conduction velocity. This development enhanced the efficiency of distributed neural networks, expanding the transfer of information throughout the brain (5). Information transfer serves to complement the information processing of gray matter, where neuronal cell bodies, synapses, and a variety of neurotransmitters are located (5). The result is a brain with prodigious numbers of both neurons and myelinated axons, which have evolved to subserve the domains of attention, memory, emotion, language, perception, visuospatial processing, executive function (5), and social cognition (7). © 2021 American Association for the Advancement of Science.

Keyword: Development of the Brain; Attention
Link ID: 27862 - Posted: 06.19.2021

By Laura Sanders Some big scientific discoveries aren’t actually discovered. They are borrowed. That’s what happened when scientists enlisted proteins from an unlikely lender: green algae. Cells of the algal species Chlamydomonas reinhardtii are decorated with proteins that can sense light. That ability, first noticed in 2002, quickly caught the attention of brain scientists. A light-sensing protein promised the power to control neurons — the brain’s nerve cells — by providing a way to turn them on and off, in exactly the right place and time. Nerve cells genetically engineered to produce the algal proteins become light-controlled puppets. A flash of light could induce a quiet neuron to fire off signals or force an active neuron to fall silent. “This molecule is the light sensor that we needed,” says vision neuroscientist Zhuo-Hua Pan, who had been searching for a way to control vision cells in mice’s retinas. The method enabled by these loaner proteins is now called optogenetics, for its combination of light (opto) and genes. In less than two decades, optogenetics has led to big insights into how memories are stored, what creates perceptions and what goes wrong in the brain during depression and addiction. Using light to drive the activity of certain nerve cells, scientists have toyed with mouse hallucinations: Mice have seen lines that aren’t there and have remembered a room they had never been inside. Scientists have used optogenetics to make mice fight, mate and eat, and even given blind mice sight. In a big first, optogenetics recently restored aspects of a blind man’s vision. © Society for Science & the Public 2000–2021.

Keyword: Brain imaging; Learning & Memory
Link ID: 27861 - Posted: 06.19.2021

Scientists studied the brain activity of school-aged children during development and found that regions that activated upon seeing limbs (hands, legs, etc.) subsequently activated upon seeing faces or words when the children grew older. The research, by scientists at Stanford University, Palo Alto, California, reveals new insights about vision development in the brain and could help inform prevention and treatment strategies for learning disorders. The study was funded by the National Eye Institute and is published in Nature Human Behaviour. “Our study addresses how experiences, such as learning to read, shape the developing brain,” said Kalanit Grill-Spector, Ph.D., a professor at Stanford University’s Wu Tsai Neurosciences Institute. “Further, it sheds light on the initial functional role of brain regions that later in development process written words, before they support this important skill of reading.” Grill-Spector’s team used functional MRI to study areas in the ventral temporal cortex (VTC) that are stimulated by the recognition of images. About 30 children, ages 5 to 12 at their first MRI, participated in the study. While in the MRI scanner, the children viewed images from 10 different categories, including words, body parts, faces, objects, and places. The researchers mapped areas of VTC that exhibited stimulation and measured how they changed in intensity and volume on the children’s subsequent MRI tests over the next one to five years. Results showed that VTC regions corresponding to face and word recognition increased with age. Compared to the 5-9-year-olds, teenagers had twice the volume of the word-selective region in VTC. Notably, as word-selective VTC volume doubled, limb-selective volume in the same region halved. According to the investigators, the decrease in limb-selectivity is directly linked to the increase in word- and face-selectivity, providing the first evidence for cortical recycling during childhood development.

Keyword: Vision; Development of the Brain
Link ID: 27860 - Posted: 06.19.2021

By Lenny Bernstein MORGANTOWN, W.Va. — After nearly two decades of hardcore drug addiction — after overdoses and rehabs and relapses, homelessness and dead friends and ruined lives — Gerod Buckhalter had one choice left, and he knew it. He could go on the same way and die young in someone’s home or a parking lot, another casualty in a drug epidemic that has claimed nearly 850,000 people like him. Or he could let a surgeon cut two nickel-size holes in his skull and plunge metal-tipped electrodes into his brain. More than 600 days after he underwent the experimental surgery, Buckhalter has not touched drugs again — an outcome so outlandishly successful that neither he nor his doctors dared hope it could happen. He is the only person in the United States to ever have substance use disorder relieved by deep brain stimulation. The procedure has reversed Parkinson’s disease, epilepsy and a few other intractable conditions, but had never been attempted for drug addiction here. The device, known as a deep brain stimulator, also is recording the electrical activity in Buckhalter’s brain — another innovation that researchers hope will help locate a biomarker for addiction and allow earlier intervention with other people. Buckhalter, 35, is a walking, talking laboratory for the outer edge of drug addiction therapy, a living experiment in what may be possible someday. Yet for all the futuristic prospects, he is also proof of how difficult treatment of addiction remains. Quelling it with a scalpel helps refute the false belief that substance use disorder is a weakness or a moral failing, rather than a brain disease. But it does not address the psychological, social and socioeconomic factors that complicate the disease.

Keyword: Drug Abuse
Link ID: 27859 - Posted: 06.19.2021

Laura Sanders A new view of the human brain shows its cellular residents in all their wild and weird glory. The map, drawn from a tiny piece of a woman’s brain, charts the varied shapes of 50,000 cells and 130 million connections between them. This intricate map, named H01 for “human sample 1,” represents a milestone in scientists’ quest to provide ever more detailed descriptions of a brain (SN: 2/7/14). “It’s absolutely beautiful,” says neuroscientist Clay Reid at the Allen Institute for Brain Science in Seattle. “In the best possible way, it’s the beginning of something very exciting.” Scientists at Harvard University, Google and elsewhere prepared and analyzed the brain tissue sample. Smaller than a sesame seed, the bit of brain was about a millionth of an entire brain’s volume. It came from the cortex — the brain’s outer layer responsible for complex thought — of a 45-year-old woman undergoing surgery for epilepsy. After it was removed, the brain sample was quickly preserved and stained with heavy metals that revealed cellular structures. The sample was then sliced into more than 5,000 wafer-thin pieces and imaged with powerful electron microscopes. Computational programs stitched the resulting images back together and artificial intelligence programs helped scientists analyze them. A short description of the resulting view was published as a preprint May 30 to bioRxiv.org. The full dataset is freely available online. black background with green and purple nerve cells with lots of long tendrils These two neurons are mirror symmetrical. It’s unclear why these cells take these shapes. Lichtman Lab/Harvard University, Connectomics Team/Google For now, researchers are just beginning to see what’s there. “We have really just dipped our toe into this dataset,” says study coauthor Jeff Lichtman, a developmental neurobiologist at Harvard University. Lichtman compares the brain map to Google Earth: “There are gems in there to find, but no one can say they’ve looked at the whole thing.” © Society for Science & the Public 2000–2021.

Keyword: Brain imaging
Link ID: 27858 - Posted: 06.16.2021

By Deborah Schoch Marcel Kuttab first sensed something was awry while brushing her teeth a year ago, several months after recovering from Covid-19. Her toothbrush tasted dirty, so she threw it out and got a new one. Then she realized the toothpaste was at fault. Onions and garlic and meat tasted putrid, and coffee smelled like gasoline — all symptoms of the once little-known condition called parosmia that distorts the senses of smell and taste. Dr. Kuttab, 28, who has a pharmacy doctoral degree and works for a drug company in Massachusetts, experimented to figure out what foods she could tolerate. “You can spend a lot of money in grocery stores and land up not using any of it,” she said. The pandemic has put a spotlight on parosmia, spurring research and a host of articles in medical journals. Membership has swelled in existing support groups, and new ones have sprouted. A fast-growing British-based Facebook parosmia group has more than 14,000 members. And parosmia-related ventures are gaining followers, from podcasts to smell training kits. Yet a key question remains unanswered: How long does Covid-linked parosmia last? Scientists have no firm timelines. Of five patients interviewed for this article, all of whom first developed parosmia symptoms in late spring and early summer of last year, none has fully regained normal smell and taste. Brooke Viegut, whose parosmia began in May 2020, worked for an entertainment firm in New York City before theaters were shuttered. She believes she caught Covid in March during a quick business trip to London, and, like many other patients, she lost her sense of smell. Before she regained it completely, parosmia set in, and she could not tolerate garlic, onions or meat. Even broccoli, she said at one point earlier this year, had a chemical smell. She still can’t stomach some foods, but she is growing more optimistic. “A lot of fruits taste more like fruit now instead of soap,” she said. And she recently took a trip without getting seriously nauseous. “So, I’d say that’s progress.” © 2021 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Neuroimmunology
Link ID: 27857 - Posted: 06.16.2021

Adrienne Matei Asked about the future of Parkinson’s disease in the US, Dr Ray Dorsey says, “We’re on the tip of a very, very large iceberg.” Dorsey, a neurologist at the University of Rochester Medical Center and author of Ending Parkinson’s Disease, believes a Parkinson’s epidemic is on the horizon. Parkinson’s is already the fastest-growing neurological disorder in the world; in the US, the number of people with Parkinson’s has increased 35% the last 10 years, says Dorsey, and “We think over the next 25 years it will double again.” Most cases of Parkinson’s disease are considered idiopathic – they lack a clear cause. Yet researchers increasingly believe that one factor is environmental exposure to trichloroethylene (TCE), a chemical compound used in industrial degreasing, dry-cleaning and household products such as some shoe polishes and carpet cleaners. Advertisement Employers think the pandemic was a time for earnest self-improvement. Screw that | Jessa Crispin To date, the clearest evidence around the risk of TCE to human health is derived from workers who are exposed to the chemical in the work-place. A 2008 peer-reviewed study in the Annals of Neurology, for example, found that TCE is “a risk factor for parkinsonism.” And a 2011 study echoed those results, finding “a six-fold increase in the risk of developing Parkinson’s in individuals exposed in the workplace to trichloroethylene (TCE).” Dr Samuel Goldman of The Parkinson’s Institute in Sunnyvale, California, who co-led the study, which appeared in the Annals of Neurology journal, wrote: “Our study confirms that common environmental contaminants may increase the risk of developing Parkinson’s, which has considerable public health implications.” It was off the back of studies like these that the US Department of Labor issued a guidance on TCE, saying: “The Board recommends [...] exposures to carbon disulfide (CS2) and trichloroethylene (TCE) be presumed to cause, contribute, or aggravate Parkinsonism.” © 2021 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 27856 - Posted: 06.16.2021

Andrew Anthony David Eagleman, 50, is an American neuroscientist, bestselling author and presenter of the BBC series The Brain, as well as co-founder and chief executive officer of Neosensory, which develops devices for sensory substitution. His area of speciality is brain plasticity, and that is the subject of his new book, Livewired, which examines how experience refashions the brain, and shows that it is a much more adaptable organ than previously thought. For the past half-century or more the brain has been spoken of in terms of a computer. What are the biggest flaws with that particular model? It’s a very seductive comparison. But in fact, what we’re looking at is three pounds of material in our skulls that is essentially a very alien kind of material to us. It doesn’t write down memories, the way we think of a computer doing it. And it is capable of figuring out its own culture and identity and making leaps into the unknown. I’m here in Silicon Valley. Everything we talk about is hardware and software. But what’s happening in the brain is what I call livewire, where you have 86bn neurons, each with 10,000 connections, and they are constantly reconfiguring every second of your life. Even by the time you get to the end of this paragraph, you’ll be a slightly different person than you were at the beginning. In what way does the working of the brain resemble drug dealers in Albuquerque? It’s that the brain can accomplish remarkable things without any top-down control. If a child has half their brain removed in surgery, the functions of the brain will rewire themselves on to the remaining real estate. And so I use this example of drug dealers to point out that if suddenly in Albuquerque, where I happened to grow up, there was a terrific earthquake, and half the territory was lost, the drug dealers would rearrange themselves to control the remaining territory. It’s because each one has competition with his neighbours and they fight over whatever territory exists, as opposed to a top-down council meeting where the territory is distributed. And that’s really the way to understand the brain. It’s made up of billions of neurons, each of which is competing for its own territory. © 2021 Guardian News & Media Limited

Keyword: Development of the Brain; Stroke
Link ID: 27855 - Posted: 06.16.2021

Dr Rocio Camacho Morales A transparent metallic film allowing a viewer to see in the dark could one day turn regular spectacles into night vision googles. The ultra-thin film, made of a semiconductor called gallium arsenide, could also be used to develop compact and flexible infrared sensors, scientists say. Though still a proof of concept, the researchers believe it could eventually be turned into a cheap and lightweight replacement for bulky night-vision goggles, which are used in military, police and security settings. The film was developed by a team of Australian and European researchers, with details published in the journal Advanced Photonics. It works by converting infrared light – which is normally invisible to humans – into light visible to the human eye. The study’s first author, Dr Rocio Camacho Morales of the Australian National University, said the material was hundreds of times thinner than a strand of human hair. The gallium arsenide is arranged in a crystalline structure only several hundred nanometres thick, which allows visible light to pass through it. The film has certain similarities to night vision goggles. Blind man has sight partly restored after pioneering treatment Read more “The way these night vision goggles work [is] they also pick up infrared light,” said Camacho Morales. “This infrared light is converted to electrons and displayed [digitally]. In our case, we’re not doing this.” Instead, the film, which does not require any power source, changes the energy of photons of light passing through it, in what is known as a nonlinear optical process. One likely advantage of this film over existing technologies is weight: bulky helmet-mounted night vision goggles have previously been associated with neck pain in airforce pilots, for example. Photons of infrared light have very low energy, Camacho Morales said, which means that electronic night vision devices can be affected by random fluctuations in signal. To minimise these fluctuations, many infrared imaging devices use cooling systems, sometimes requiring cryogenic temperatures. © 2021 Guardian News & Media Limited

Keyword: Vision
Link ID: 27854 - Posted: 06.16.2021

By Carolyn Wilke Scientists have long sought to prevent sharp memories from dulling with age, but the problem remains stubborn. Now research published in Scientific Reports suggests virtual reality might help older people recall facts and events based on specific details. The study involved 42 healthy older adults from the San Francisco Bay Area. Half spent a dozen hours over four weeks playing a virtual-reality game called Labyrinth; they strapped on headsets and walked in place, roaming virtual neighborhoods while completing errands. The other half, in the control group, used electronic tablets to play games that did not require navigating or recalling details. After 15 sessions, the latter performed roughly the same as before on a long-term memory test based on picking out objects they had seen about an hour earlier. But the Labyrinth players' scores rose, and they were less frequently tricked by objects that resembled ones they had viewed. Those improvements “brought them back up to the level of another group of younger adults who did the same memory tests,” says cognitive neuroscientist Peter Wais of the University of California, San Francisco. He and his colleagues designed the VR game, which they say likely stimulates the hippocampus—a brain area important for long-term memory. The team did not observe improvement on two other tests, which measured autobiographical memory and spatial memory capability. © 2021 Scientific American,

Keyword: Learning & Memory; Alzheimers
Link ID: 27853 - Posted: 06.16.2021

Ed Yong Carl Schoonover and Andrew Fink are confused. As neuroscientists, they know that the brain must be flexible but not too flexible. It must rewire itself in the face of new experiences, but must also consistently represent the features of the external world. How? The relatively simple explanation found in neuroscience textbooks is that specific groups of neurons reliably fire when their owner smells a rose, sees a sunset, or hears a bell. These representations—these patterns of neural firing—presumably stay the same from one moment to the next. But as Schoonover, Fink, and others have found, they sometimes don’t. They change—and to a confusing and unexpected extent. Schoonover, Fink, and their colleagues from Columbia University allowed mice to sniff the same odors over several days and weeks, and recorded the activity of neurons in the rodents’ piriform cortex—a brain region involved in identifying smells. At a given moment, each odor caused a distinctive group of neurons in this region to fire. But as time went on, the makeup of these groups slowly changed. Some neurons stopped responding to the smells; others started. After a month, each group was almost completely different. Put it this way: The neurons that represented the smell of an apple in May and those that represented the same smell in June were as different from each other as those that represent the smells of apples and grass at any one time. This is, of course, just one study, of one brain region, in mice. But other scientists have shown that the same phenomenon, called representational drift, occurs in a variety of brain regions besides the piriform cortex. Its existence is clear; everything else is a mystery. Schoonover and Fink told me that they don’t know why it happens, what it means, how the brain copes, or how much of the brain behaves in this way. How can animals possibly make any lasting sense of the world if their neural responses to that world are constantly in flux? (c) 2021 by The Atlantic Monthly Group

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27852 - Posted: 06.11.2021

By Carl Zimmer Dr. Adam Zeman didn’t give much thought to the mind’s eye until he met someone who didn’t have one. In 2005, the British neurologist saw a patient who said that a minor surgical procedure had taken away his ability to conjure images. Over the 16 years since that first patient, Dr. Zeman and his colleagues have heard from more than 12,000 people who say they don’t have any such mental camera. The scientists estimate that tens of millions of people share the condition, which they’ve named aphantasia, and millions more experience extraordinarily strong mental imagery, called hyperphantasia. In their latest research, Dr. Zeman and his colleagues are gathering clues about how these two conditions arise through changes in the wiring of the brain that join the visual centers to other regions. And they’re beginning to explore how some of that circuitry may conjure other senses, such as sound, in the mind. Eventually, that research might even make it possible to strengthen the mind’s eye — or ear — with magnetic pulses. “This is not a disorder as far as I can see,” said Dr. Zeman, a cognitive scientist at the University of Exeter in Britain. “It’s an intriguing variation in human experience.” The patient who first made Dr. Zeman aware of aphantasia was a retired building surveyor who lost his mind’s eye after minor heart surgery. To protect the patient’s privacy, Dr. Zeman refers to him as M.X. When M.X. thought of people or objects, he did not see them. And yet his visual memories were intact. M.X. could answer factual questions such as whether former Prime Minister Tony Blair has light-colored eyes. (He does.) M.X. could even solve problems that required mentally rotating shapes, even though he could not see them. I came across M.X.’s case study in 2010 and wrote a column about it for Discover magazine. Afterward, I got emails from readers who had the same experience but who differed from M.X. in a remarkable way: They had never had a mind’s eye to begin with. © 2021 The New York Times Company

Keyword: Attention; Vision
Link ID: 27851 - Posted: 06.11.2021

By Emily Underwood In the 1930s, neurosurgeon Wilder Penfield pioneered a daring new kind of cartography. As a stenographer took notes, he delicately touched an electrode to the exposed brains of his awake, consenting patients and asked what they felt as electrical current hit different areas. Penfield wanted to better predict which brain functions would be threatened when surgeons had to remove tumors or chunks of tissue that were triggering epileptic seizures. Stimulating adjacent brain regions, he found, produced sensations in corresponding body parts: hand, forearm, elbow. The result of his mapping was the iconic “homunculus”: a map on the brain’s wrinkled outer layer representing the surface of the body. Penfield then ventured into more mysterious territory. When he probed the insula, a deep fold of cortex, some patients felt nauseated or gassy; others belched or vomited. “My stomach is upset and I smell something like medicine,” one said. Penfield found those visceral signals harder to decipher than the brain’s map of the body’s surface. Brain regions responsible for different internal sensations seemed to overlap. Sensory regions were hard to distinguish from those that sent motor instructions such as telling the intestines to contract. Penfield once asked participants to swallow an electrode to detect changes in gut contractions while he stimulated their brains. But his map of the inner organs was blurry and ambiguous—and stayed that way for most of the next century. Decades later, scientists are starting to unravel how our wet, spongy, slippery organs talk to the brain and how the brain talks back. That two-way communication, known as interoception, encompasses a complex, bodywide system of nerves and hormones. Much recent exploration has focused on the vagus nerve: a massive, meandering network of more than 100,000 fibers that travel from nearly every internal organ to the base of the brain and back again. © 2021 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 27850 - Posted: 06.11.2021

By Pam Belluck and Rebecca Robbins In a powerful statement of disagreement with the Food and Drug Administration’s approval of Biogen’s controversial Alzheimer’s drug, three scientists have resigned from the independent committee that advised the agency on the treatment. “This might be the worst approval decision that the F.D.A. has made that I can remember,” said Dr. Aaron Kesselheim, a professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, who submitted his resignation Thursday after six years on the committee. He said the agency’s approval of the drug, aducanumab, which is being marketed as Aduhelm, a monthly intravenous infusion that Biogen has priced at $56,000 per year, was wrong “because of so many different factors, starting from the fact that there’s no good evidence that the drug works.” Two other members of the committee resigned earlier this week, expressing dismay at the approval of the drug despite the committee’s overwhelming rejection of it after reviewing clinical trial data in November. The committee had found that the evidence did not convincingly show that Aduhelm could slow cognitive decline in people in the early stages of the disease — and that the drug could cause potentially serious side effects of brain swelling and brain bleeding. None of the 11 members of the committee considered the drug ready for approval: Ten voted against and one was uncertain. “Approval of a drug that is not effective has serious potential to impair future research into new treatments that may be effective,” said Dr. Joel Perlmutter, a neurologist at Washington University School of Medicine in St. Louis, who was the first to resign from the committee. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 27849 - Posted: 06.11.2021

Ian Sample Science editor Regular strenuous exercise raises the risk of developing motor neurone disease (MND) in people who are genetically predisposed to the condition, researchers say. Scientists at the University of Sheffield found a causal relationship between high intensity physical activity and the disorder among those already susceptible to the disease. They believe the work marks a major step towards understanding the link between intense exercise, which may contribute to motor neurone injury in certain people, and the neurodegenerative disease, which affects about 5,000 individuals in the UK. “We have suspected for some time that exercise was a risk factor for MND, but until now this link was considered controversial,” said Dr Johnathan Cooper-Knoc, a neurologist at Sheffield. “This study confirms that in some people, frequent strenuous exercise leads to an increase in the risk of MND.” The life-time risk of developing MND is about 1 in 400, but previous studies have suggested it is six times greater in professional football players compared with the general population. A number of high-profile British sportsmen have shared their experience with MND in recent years, including rugby league’s Rob Burrow, rugby union’s Doddie Weir and the the footballer Stephen Darby. The Sheffield researchers emphasise that the vast majority of people who undertake vigorous exercise do not develop MND, and that their next step is to develop tests that identify people most at risk. © 2021 Guardian News & Media Limited

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27848 - Posted: 06.11.2021

By Anahad O'Connor According to recent studies, the number of people complaining of insomnia skyrocketed during the pandemic, rising from 20 percent of adults last summer to nearly 60 percent in March. If you’re one of those people who’s been plagued by poor sleep, the Well desk is here to help. Recently, we asked our readers to tell us two things: What’s keeping you from getting a good night’s rest? And what are the most pressing questions you would ask a sleep expert? More than 1,200 of you responded. You asked about insomnia, supplements, middle-of-the-night awakenings, snoring bed mates and more. So we collected your most popular questions, brought them to the world’s top sleep experts and shared their answers below. Sometimes I am physically tired but can’t fall asleep. How is that possible? This is what’s known as the tired but wired syndrome. Usually, it’s driven by stress and anxiety. Even if you’re exhausted, a racing mind can activate the “fight or flight” branch of your nervous system, making you alert and unable to fall asleep. “For us to fall asleep and stay asleep, we need to go in the opposite nervous system direction,” said Matthew Walker, a professor of neuroscience and psychology at the University of California, Berkeley, and the author of the best-selling book “Why We Sleep.” “We need to shift over to the calming branch of the nervous system called the parasympathetic nervous system.” © 2021 The New York Times Company

Keyword: Sleep
Link ID: 27847 - Posted: 06.11.2021

By Laurie McGinley The Food and Drug Administration on Monday approved the first Alzheimer’s treatment intended to slow cognitive decline, a move hailed by patients and advocates but sharply criticized by others who argued there was not sufficient evidence that the drug works. The medication, called aducanumab, is the first drug cleared for Alzheimer’s that is designed to alter the course of the disease by slowing the deterioration of brain function — not just to ease symptoms. No Alzheimer’s treatment has been approved since 2003, reflecting the extraordinarily high failure rate of drugs developed for the illness. But in an explicit acknowledgment of the uncertainties about the effectiveness of the drug, the FDA did not grant the medication full approval. Instead, the agency cleared the drug — its brand name will be Aduhelm — based on its ability to reduce clumps of amyloid beta in the brain, a hallmark of the disease. It ordered the drug’s maker, the biotech giant Biogen, to conduct a post-approval study confirming the medicine actually slows cognitive deterioration. If the medication does not provide such a clinical benefit, the FDA’s approval could be withdrawn. Patrizia Cavazzoni, director of the FDA’s Center for Drug Evaluation and Research, said officials believe it is “reasonably likely” that the reduction in amyloid clumps will confer “important benefits to patients.” Monday’s FDA decision was the most contentious in years and followed prolonged debate among researchers, doctors, patients and advocates about whether the medication works — a consequence of the drug’s complicated history. One of the biggest points of disagreement is whether a reduction in amyloid beta, a sticky compound that many scientists believe damages communication between brain cells and eventually kills them, results in a slowdown in cognitive decline. © 1996-2021 The Washington Post

Keyword: Alzheimers
Link ID: 27846 - Posted: 06.08.2021