A new study in Neuron offers clues to why autism spectrum disorder (ASD) is more common in boys than in girls. National Institutes of Health scientists found that a single amino acid change in the NLGN4 gene, which has been linked to autism symptoms, may drive this difference in some cases. The study was conducted at NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Researchers led by Katherine Roche, Ph.D., a neuroscientist at NINDS, compared two NLGN4 genes, (one on the X chromosome and one on the Y chromosome), which are important for establishing and maintaining synapses, the communication points between neurons. Every cell in our body contains two sex chromosomes. Females have two X chromosomes; males have one X and one Y chromosome. Until now, it was assumed that the NLGN4X and NLGN4Y genes, which encode proteins that are 97% identical, functioned equally well in neurons. But using a variety of advanced technology including biochemistry, molecular biology, and imaging tools, Dr. Roche and her colleagues discovered that the proteins encoded by these genes display different functions. The NLGN4Y protein is less able to move to the cell surface in brain cells and is therefore unable to assemble and maintain synapses, making it difficult for neurons to send signals to one another. When the researchers fixed the error in cells in a dish, they restored much of its correct function. “We really need to look at NLGN4X and NLGN4Y more carefully,” said Thien A. Nguyen, Ph.D., first author of the study and former graduate student in Dr. Roche’s lab.

Keyword: Autism; Genes & Behavior
Link ID: 27165 - Posted: 04.03.2020

By Roni Caryn Rabin Neurologists around the world say that a small subset of patients with Covid-19 are developing serious impairments of the brain. Although fever, cough and difficulty breathing are the typical hallmarks of infection with the new coronavirus, some patients exhibit altered mental status, or encephalopathy, a catchall term for brain disease or dysfunction that can have many underlying causes, as well as other serious conditions. These neurological syndromes join other unusual symptoms, such as diminished sense of smell and taste as well as heart ailments. In early March, a 74-year-old man came to the emergency room in Boca Raton, Fla., with a cough and a fever, but an X-ray ruled out pneumonia and he was sent home. The next day, when his fever spiked, family members brought him back. He was short of breath, and could not tell doctors his name or explain what was wrong — he had lost the ability to speak. The patient, who had chronic lung disease and Parkinson’s, was flailing his arms and legs in jerky movements, and appeared to be having a seizure. Doctors suspected he had Covid-19, and were eventually proven right when he was finally tested. On Tuesday, doctors in Detroit reported another disturbing case involving a female airline worker in her late 50s with Covid-19. She was confused, and complained of a headache; she could tell the physicians her name but little else, and became less responsive over time. Brain scans showed abnormal swelling and inflammation in several regions, with smaller areas where some cells had died. Physicians diagnosed a dangerous condition called acute necrotizing encephalopathy, a rare complication of influenza and other viral infections. “The pattern of involvement, and the way that it rapidly progressed over days, is consistent with viral inflammation of the brain,” Dr. Elissa Fory, a neurologist with Henry Ford Health System, said through an email. “This may indicate the virus can invade the brain directly in rare circumstances.” The patient is in critical condition. © 2020 The New York Times Company

Keyword: Neuroimmunology; Stroke
Link ID: 27164 - Posted: 04.03.2020

By Bruce Bower Lucy’s kind had small, chimplike brains that, nevertheless, grew at a slow, humanlike pace. This discovery, reported April 1 in Science Advances, shows for the first time that prolonged brain growth in hominid youngsters wasn’t a by-product of having unusually large brains. An influential idea over the last 20 years has held that extended brain development after birth originated in the Homo genus around 2.5 million years ago, so that mothers — whose pelvic bones and birth canal had narrowed to enable efficient upright walking — could safely deliver babies. But Australopithecus afarensis, an East African hominid species best known for Lucy’s partial skeleton, also had slow-developing brains that reached only about one-third the volume of present-day human brains, say paleoanthropologist Philipp Gunz of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, and his colleagues. And A. afarensis is roughly 3 million to 4 million years old, meaning slow brain growth after birth developed before members of the Homo genus appeared, perhaps as early as 2.8 million years ago (SN: 3/4/15). Too few A. afarensis infants have been studied to calculate the age at which this species attained adult-sized brains, Gunz cautions. The brains of human infants today reach adult sizes by close to age 5, versus an age of around 2 or 3 for both chimps and gorillas. In the new study, Gunz and colleagues estimated brain volumes for six A. afarensis adults and two children, estimated to have been about 2 years and 5 months old. The kids had brains that were smaller than adult A. afarensis brain sizes in a proportion similar to human children’s brains at the same age relative to adult humans. © Society for Science & the Public 2000–2020.

Keyword: Evolution; Development of the Brain
Link ID: 27163 - Posted: 04.02.2020

Emiliano Rodríguez Mega On a cold Friday night in February 1995, addiction researcher Nora Volkow and her husband got into their car after a long day at Brookhaven National Laboratory in Upton, New York. Ice had covered the trees and the roads, making them sparkle. But as the couple drove down a slope, the tyres lost their grip. The vehicle spun out of control. Volkow curled up to shield herself as an oncoming car crashed into her door. Metal bit into her flesh. The pain was unrelenting. Finally, the fire service arrived to break her free and an ambulance rushed her to the nearest emergency department, where a doctor gave her Demerol, a powerful and highly addictive opioid painkiller also known as pethidine, which is similar to morphine. Volkow had spent countless hours talking to people with addiction and had read hundreds of papers on the mechanisms of drug abuse. Neither prepared her for what happened next. “It was extraordinary, those impressive sensations,” she says. A moment of ecstasy, one she describes as comparable only to long-lasting sexual pleasure, eclipsed all other feelings. She stayed on the medication for another few days and was sent home with more. But she decided not to take it. She was afraid — she knew many of her patients could not stop once they started. She would get through the pain without the help of drugs. © 2020 Springer Nature Limited

Keyword: Drug Abuse; Pain & Touch
Link ID: 27162 - Posted: 04.02.2020

By Jennifer Szalai Donald Galvin was a sophomore at Colorado State when he first checked into the campus health clinic to get treated for a cat bite, offering no further explanation of what had occurred. Two years and several visits later, he arrived at the clinic with another cat bite — only this time he told a doctor what happened to the cat. “He killed a cat slowly and painfully,” the doctor recorded in his notes. “Doesn’t know why he killed the cat nor why he tormented. Got emotionally upset as he discussed the behavior.” The oldest of 12 siblings, Donald was the first to be told he was schizophrenic. Five of his brothers would eventually get the same diagnosis. Even the healthy children in the Galvin family were beset in a sense, forced to live with an affliction that inevitably shaped their relationships to their parents and to one another. As the journalist Robert Kolker writes in “Hidden Valley Road,” having just one schizophrenic family member is bound to reorient the experiences of everyone else; having six made the Galvins extraordinary, not least to the medical researchers who eventually studied them. Kolker’s previous book, “Lost Girls,” traced the lives of five murdered women on Long Island and told a story of sex work and law enforcement during a time of technological change. His new book is a comparable feat of empathy and narrative journalism, as he coaxes out the struggles of the Galvin family, showing how they embodied the roiling debates over the science of schizophrenia — not just its causes, “but what it actually is.” The Galvin children were all born between 1945 and 1965, during the two decades of the baby boom. It was a time when the psychoanalytic approach to mental illness, with its theory of the cold and domineering “schizophrenogenic mother,” reigned supreme. What began as a more holistic rejoinder to the crude biological reductionism of the early 20th century soon hardened into its own orthodoxy. According to its proponents, mental illness was a disease of nurture, not nature; as one psychiatrist put it, the schizophrenic patient “is always one who is reared by a woman who suffers from a perversion of the maternal instinct.” © 2020 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27161 - Posted: 04.02.2020

Kristen Jordan Shamus, Detroit Free Press A 58-year-old woman hospitalized in the Henry Ford Health System who has the new coronavirus developed a rare complication: encephalitis. In a case report published online Tuesday in the journal Radiology, a team of doctors say the woman tested positive for the coronavirus, but also developed a case of acute necrotizing encephalitis, or ANE, a central nervous infection that mostly afflicts young children. It is believed to be the first published case linking COVID-19 and acute necrotizing encephalitis. The rare and serious brain disease can develop in people who have a viral infection, and causes lesions to form in the brain, tissue death and symptoms such as seizures, drowsiness, confusion and coma. The woman, who was identified as an airline worker, had several days of fever, cough and muscle aches, and was taken by ambulance March 19 to a Henry Ford emergency room, said Dr. Elissa Fory, a Henry Ford neurologist. The patient also showed signs of confusion, lethargy and disorientation. A flu test turned up negative but a rapid COVID-19 test, developed in-house by Henry Ford’s clinical microbiology lab, confirmed she had the coronavirus, Fory said. When the woman remained lethargic, doctors ordered repeat CT and MRI scans, which revealed abnormal lesions in both thalami and temporal lobes, parts of the brain that control consciousness, sensation and memory function. These scans confirmed doctors’ early suspicions.

Keyword: Miscellaneous
Link ID: 27160 - Posted: 04.02.2020

By Robert Frederick An early sign of neurodegenerative disease at the cellular level is often the loss of integrity in axons, the threadlike part of neurons that conduct impulses. To find out what causes that loss of integrity, researchers have been trying to better understand the axon’s lining, called the membrane-associated periodic scaffold (MPS). If neuroscientists can discover what signals the MPS to disassemble, they may gain an early diagnostic tool for neurodegenerative diseases or a new target for drug therapy. Back in 2013, researchers using advanced optical microscopy identified the presence of rings in the MPS made from the protein actin. At first, the discovery was met with skepticism because no one had seen the rings using electron microscopes, which have more resolution than optical methods. But preparing neurons for electron microscopy often involves dissolving the membrane with a surfactant. “If you remove completely the membrane, you also disorganize the scaffold that is very tightly associated with the membrane,” says Christophe Leterrier, a neuro-biologist at Aix-Marseille Université in France. To see the periodic rings (shown above in orange at increasing levels of zoom) Leterrier combined optical and electron microscopy. Just as previous researchers had done to visualize the MPS, the first step involved a technique called unroofing a cell, which can isolate a cell’s membrane without disorganizing the underlying scaffold. But the researchers then used electron microscopy to image the same unroofed axon: Teamed up with Stéphane Vassilopoulos, Leterrier’s group essentially made a platinum replica of the MPS and used electron microscopy (shown above in grayscale) on the replica “to really see individual proteins.” The researchers published their findings in Nature Communications, discovering that the rings are like braided wreaths made from long actin filaments. Leterrier says the next step is to find what signal will prompt the MPS to disassemble but will not affect a neuron’s other actin structures, such as dendritic spines, which receive other neurons’ signals. © 2020 Sigma Xi, The Scientific Research Honor Society

Keyword: Brain imaging
Link ID: 27159 - Posted: 04.02.2020

Abby Olena Nicole Ward, who studies inflammatory skin diseases at Case Western Reserve University, was all set to ship the last six mice in a cohort to a collaborator at the University of Michigan for analysis next week. But then she got word that the University of Michigan would no longer accept any animals, as the university scaled back operations to only essential research to limit the number of people on campus and protect the community from COVID-19. Case Western followed with similar reductions in in-person research activities. “We’re lucky,” Ward says. “What we’ve been told is: don’t start any new experiments, but you’re allowed to continue the experiments that you have ongoing.” That’s not the case everywhere. About three weeks ago, Sarah Gaffen, an immunologist at the University of Pittsburgh, told her lab members to start shutting down experiments out of concern for their safety as the virus spread. On March 18, that reduction was formalized in a message from administrators at Pitt mandating that non-essential research stop two days later. “We are basically shuttered. We stopped everything except for minimal mouse maintenance,” she says. “We’re not allowed to buy them. We’re not allowed to breed them up.” Bianca Coleman, Gaffen’s lab manager, continues to report to work to care for the mouse colonies. But she is also taking steps to shrink the population, so that if she or the university’s animal care workers get sick, the mice that remain can be supervised by fewer people. Since the cut backs started, she’s reduced the colonies by about 80 cages, which might each have a handful of mice, and still expects to make further reductions of the 300–400 cages she typically oversees, she tells The Scientist in an email. © 1986–2020 The Scientist

Keyword: Animal Rights
Link ID: 27158 - Posted: 04.01.2020

By Michelle Roberts Health editor, BBC News online A loss of smell or taste may be a sign that you have coronavirus, according to UK researchers. A team at King's College London looked at responses from more than 400,000 people reporting suspected Covid-19 symptoms to an app. But loss of smell and taste are also signs of other respiratory infections, such as the common cold. And experts say fever and cough remain the most important symptoms of the virus to look out for and act upon. If you or someone you live with has a new continuous cough or high temperature, the advice is stay at home to stop the risk of spreading coronavirus to others. Coronavirus: What should I do? What did the study find? The King's College researchers wanted to gather information on possible coronavirus symptoms to help experts better understand and fight the disease. Of those reporting one or more symptoms of coronavirus to the Covid Symptom Tracker app: 53% said they had fatigue or tiredness 29% persistent cough 28% shortness of breath 18% loss of sense of smell or taste 10.5% suffered from fever Of these 400,000 people, 1,702 said they had been tested for Covid-19, with 579 receiving a positive result and 1,123 a negative one. Among the ones who had coronavirus infection confirmed by a positive test, three-fifths (59%) reported loss of smell or taste. © 2020 BBC

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27157 - Posted: 04.01.2020

By Elizabeth Pennisi Males resort to all sorts of desperate measures when fertile females are scarce, including banding together to guard a potential mate. Now, researchers have discovered that such bands of bottlenose dolphins may coordinate their actions with unique “popping” calls—the first evidence that animals other than humans can synchronize themselves using vocal signals. Humans often use vocal signals to coordinate actions, like marching and dancing, that reinforce unity and intimidate outside groups. The synchronized displays of other animals—like fireflies that light up at the same time—are thought to be competitive, showing off which male is the sexiest, rather than cooperative. In Shark Bay, off the coast Western Australia 800 kilometers north of Perth, groups of up to 14 male dolphins form lifelong alliances. Together, subsets of three keep close tabs on potential female mates, swimming, turning, and surfacing in unison to guard and herd them—one female at a time. Scientists watching this behavior noticed these males often emit a unique “popping” call, making series of two to 49 very short sounds, 10 per second, over and over. e dolphins popping The scientists dragged four underwater microphones behind a motorboat and recorded 172 instances in which multiple males were “popping” together (above). When the males pop alone, their timing and tempo varies. But when they pop together, they do it at the same time and at the same rate, suggesting they are using the sounds to enhance their cooperation, the team reports today in the Proceedings of the Royal Society B. This synchronized popping may be a threat, as it tends to make the female dolphin move closer to her male guards. But more importantly, the researchers say, it may help reinforce that the males need to act—and talk—as one to ensure they get their gal. © 2020 American Association for the Advancement of Science

Keyword: Sexual Behavior; Aggression
Link ID: 27156 - Posted: 04.01.2020

Nicola Davis Reading minds has just come a step closer to reality: scientists have developed artificial intelligence that can turn brain activity into text. While the system currently works on neural patterns detected while someone is speaking aloud, experts say it could eventually aid communication for patients who are unable to speak or type, such as those with locked in syndrome. “We are not there yet but we think this could be the basis of a speech prosthesis,” said Dr Joseph Makin, co-author of the research from the University of California, San Francisco. Writing in the journal Nature Neuroscience, Makin and colleagues reveal how they developed their system by recruiting four participants who had electrode arrays implanted in their brain to monitor epileptic seizures. These participants were asked to read aloud from 50 set sentences multiple times, including “Tina Turner is a pop singer”, and “Those thieves stole 30 jewels”. The team tracked their neural activity while they were speaking. This data was then fed into a machine-learning algorithm, a type of artificial intelligence system that converted the brain activity data for each spoken sentence into a string of numbers. To make sure the numbers related only to aspects of speech, the system compared sounds predicted from small chunks of the brain activity data with actual recorded audio. The string of numbers was then fed into a second part of the system which converted it into a sequence of words. © 2020 Guardian News & Media Limited

Keyword: Language; Brain imaging
Link ID: 27155 - Posted: 03.31.2020

By Stephen Casper. The poet Emily Dickinson rendered the brain wider than the sky, deeper than the sea, and about the weight of God. Scientists facing the daunting task of describing this organ conventionally conjure up different kinds of metaphor — of governance; of maps, infrastructure networks and telecommunications; of machines, robots, computers and the Internet. The comparisons have been practical and abundant. Yet, perhaps because of their ubiquity, the metaphors we use to understand the brain often go unnoticed. We forget that they are descriptors, and see them instead as natural properties. Such hidden dangers are central to biologist and historian Matthew Cobb’s The Idea of the Brain. This ambitious intellectual history follows the changing understanding of the brain from antiquity to the present, mainly in Western thought. Cobb outlines a growing challenge to the usefulness of metaphor in directing and explaining neuroscience research. With refreshing humility, he contends that science is nowhere near working out what brains do and how — or even if anything is like them at all. Cobb shows how ideas about the brain have always been forged from the moral, philosophical and technological frameworks to hand for those crafting the dominant narratives of the time. In the seventeenth century, the French philosopher René Descartes imagined an animal brain acting through hydraulic mechanisms, while maintaining a view of the divine nature of a mind separate from matter. Later authorities, such as the eighteenth-century physician and philosopher Julien Offray de Le Mettrie, secularized the image and compared the human to a machine. The Italian physicist Alessandro Volta rejected the idea of ‘animal electricity’, proposed by his rival Luigi Galvani as a vital force that animates organic matter. Volta was driven at least partly by his aversion to the mechanistic view. © 2020 Springer Nature Limited

Keyword: Brain imaging
Link ID: 27154 - Posted: 03.31.2020

By Sheila Kaplan, Andrew Jacobs and Choe Sang-Hun In January 2019, the chairman of Altria, Howard A. Willard III, flew to Silicon Valley to speak to senior executives of Juul Labs, fresh off signing a deal for the tobacco giant to pay nearly $13 billion for a 35 percent stake in the popular e-cigarette company. With public fury growing over Juul’s contribution to the epidemic of teenage vaping, he laid out his vision for the company to continue to thrive. “I believe that in five years, 50 percent of Juul’s revenue will be international,” Mr. Willard told the 200 executives gathered at the Four Seasons in East Palo Alto. Kevin Burns, Juul’s chief executive at the time, interrupted: “I told the team to accomplish that in one year!” Many people in audience chuckled, but a year later, nobody is laughing. When the big American tobacco companies started feeling pressure decades ago, they found new markets and friendlier regulation abroad. Juul’s efforts to follow the same playbook have been stunningly unsuccessful. The company has been met with ferocious anti-vaping sentiment and a barrage of newly enacted e-cigarette restrictions, or outright bans, in country after country. As a result, its ambitious overseas plans have collapsed. Juul was kicked off the market in China last fall after just four days. The company has had to abandon plans for India after the government there banned all electronic cigarettes. Thailand, Singapore, Cambodia and Laos have also closed the door to e-cigarettes. In the Philippines, President Rodrigo Duterte ordered the arrest of anyone caught vaping outside designated smoking areas. Juul has postponed its launch in the Netherlands and has pulled out of Israel. In South Korea, the number of Juul customers has plummeted after the government issued dire health warnings about e-cigarettes, and the company has scaled back its distribution there. © 2020 The New York Times Company

Keyword: Drug Abuse
Link ID: 27153 - Posted: 03.31.2020

A first-of-its-kind trial has demonstrated that a receptor involved in the brain’s reward system may be a viable target for treating anhedonia (or lack of pleasure), a key symptom of several mood and anxiety disorders. This innovative fast-fail trial was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, and the results of the trial are published in Nature Medicine. Mood and anxiety disorders are some of the most commonly diagnosed mental disorders, affecting millions of people each year. Despite this, available medications are not always effective in treating these disorders. The need for new treatments is clear, but developing psychiatric medications is often a resource-intensive process with a low success rate. To address this, NIMH established the Fast-Fail Trials program with the goal of enhancing the early phases of drug development. “The fast-fail approach aims to help researchers determine — quickly and efficiently — whether targeting a specific neurobiological mechanism has the hypothesized effect and is a potential candidate for further clinical trials,” explained Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Positive results suggest that targeting a neurobiological mechanism affects brain function as expected, while negative results allow researchers to eliminate that target from further consideration. We hope this approach will pave the way towards the development of new and better treatments for individuals with mental illnesses.” In this study, researcher Andrew D. Krystal, M.D., who began the research while at the Duke University School of Medicine, Durham, North Carolina, and is now at the University of California, San Francisco, and colleagues report the first comprehensive application of this fast-fail approach. The researchers examined the kappa opioid receptor (KOR) as a possible neurobiological target for the treatment of anhedonia. Previous findings suggest that drugs that block the KOR, known as KOR antagonists, can affect reward-related brain circuits in ways that could improve reward processing and reverse anhedonia and associated symptoms.

Keyword: Depression
Link ID: 27152 - Posted: 03.31.2020

by Laura Dattaro / Mice missing an autism gene called SHANK3 respond to much lighter touches than typical mice do, according to a new study1. And this hypersensitivity seems to result from the underactivity of neurons that normally dampen sensory responses. The study is the first to examine sensory sensitivity in mice missing SHANK3. Mice with mutations in other genes tied to autism, including MECP2 and GABRB3, have also been shown to be hypersensitive to puffs of air blown onto their backs. Up to 90 percent of autistic people have sensory problems, including hypersensitivity to sensations such as sound or touch. These disruptions may underlie many of the difficulties autistic people face in navigating the world, says lead investigator Guoping Feng, professor of neuroscience at the Massachusetts Institute of Technology. “Sensory overload is one of the reasons that autistic people cover their ears, [hide] in corners, want to be quiet,” Feng says. “It’s important to understand mechanisms.” Up to 2 percent of people with autism have a mutation in SHANK3, which encodes a protein needed for neurons to communicate with one another2. Autism is also common in people with Phelan-McDermid syndrome, a condition caused by deletions of the chromosomal region in which SHANK3 is located. Other experts also say the study underscores the importance of studying sensory problems in autistic people. “Hyperreactivity to sensory input might be connected with autism in a really deep way,” says Sam Wang, professor of neuroscience at Princeton University, who was not involved in the work. “If sensory experience in the first few years of life is necessary for setting up a model of the world, an understanding of the world, then sensory processing would be a gateway to all kinds of other difficulties.” © 2020 Simons Foundation

Keyword: Autism; Attention
Link ID: 27151 - Posted: 03.30.2020

By Erika Mailman In summer 2014, when he was 54, Sacramento artist David Wetzl was exhibiting the behaviors of an elderly man with Alzheimer’s. “I have a bad brain,” he told everyone repeatedly, using a simple phrase to explain his diagnosis to the world. Two years before that, his wife, Diana Daniels, had asked for an MRI because she was suspicious that things weren’t right and fearful when he couldn’t remember the word “shoelaces.” The scan showed with horrific clarity how sections of his brain had shriveled. “The devastation began on his left temporal lobe, working its greatest damage,” says Diana. “By the time of diagnosis, his right temporal lobe also had significant atrophy.” David was diagnosed with frontotemporal dementia, or FTD, part of a group of disorders caused by nerve cell damage to the brain. The disease comes with a dispiriting prognosis. There is no cure (although symptoms can be treated), and patients usually die within seven to 13 years from the onset of symptoms. As FTD progresses, behavior can become strange and antisocial, says Matt Ozga, communications manager at the Association for Frontotemporal Degeneration in King of Prussia, Pa. Patients lose their filter and can make embarrassing remarks. For the spouses who are caught off guard, thinking their mate’s worst setback for the next few decades will be graying hair and a paunch, it’s a shock. The couple may find themselves confronted  by different challenges than those who encounter dementia later in life.

Keyword: Alzheimers
Link ID: 27150 - Posted: 03.30.2020

Stephanie Preston The media is replete with COVID-19 stories about people clearing supermarket shelves – and the backlash against them. Have people gone mad? How can one individual be overfilling his own cart, while shaming others who are doing the same? As a behavioral neuroscientist who has studied hoarding behavior for 25 years, I can tell you that this is all normal and expected. People are acting the way evolution has wired them. The word “hoarding” might bring to mind relatives or neighbors whose houses are overfilled with junk. A small percentage of people do suffer from what psychologists call “hoarding disorder,” keeping excessive goods to the point of distress and impairment. But hoarding is actually a totally normal and adaptive behavior that kicks in any time there is an uneven supply of resources. Everyone hoards, even during the best of times, without even thinking about it. People like to have beans in the pantry, money in savings and chocolates hidden from the children. These are all hoards. Most Americans have had so much, for so long. People forget that, not so long ago, survival often depended on working tirelessly all year to fill root cellars so a family could last through a long, cold winter – and still many died. Similarly, squirrels work all fall to hide nuts to eat for the rest of the year. Kangaroo rats in the desert hide seeds the few times it rains and then remember where they put them to dig them back up later. A Clark’s nutcracker can hoard over 10,000 pine seeds per fall – and even remember where it put them. © 2010–2020, The Conversation US, Inc.

Keyword: Obesity; Attention
Link ID: 27149 - Posted: 03.30.2020

Researchers at the National Institutes of Health have discovered in mice what they believe is the first known genetic mutation to improve cognitive flexibility—the ability to adapt to changing situations. The gene, KCND2, codes for a protein that regulates potassium channels, which control electrical signals that travel along neurons. The electrical signals stimulate chemical messengers that jump from neuron to neuron. The researchers were led by Dax Hoffman, Ph.D., chief of the Section on Neurophysiology at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). It appears in Nature Communications. The KCND2 protein, when modified by an enzyme, slows the generation of electrical impulses in neurons. The researchers found that altering a single base pair in the KCND2 gene enhanced the ability of the protein to dampen nerve impulses. Mice with this mutation performed better than mice without the mutation in a cognitive task. The task involved finding and swimming to a slightly submerged platform that had been moved to a new location. Mice with the mutation found the relocated platform much faster than their counterparts without the mutation. The researchers plan to investigate whether the mutation will affect neural networks in the animals’ brains. They added that studying the gene and its protein may ultimately lead to insights on the nature of cognitive flexibility in people. It also may help improve understanding of epilepsy, schizophrenia, Fragile X syndrome, and autism spectrum disorder, which all have been associated with other mutations in KCND2.

Keyword: Learning & Memory; Genes & Behavior
Link ID: 27148 - Posted: 03.30.2020

By Nicholas Bakalar There is good evidence that a daily baby aspirin reduces the risk for heart disease and stroke, and some have thought its inflammation-lowering effect might also help in delaying cognitive decline. But taking a daily low-dose aspirin did not appear to be effective in lowering the risk of Alzheimer’s disease or other forms of dementia, a new study reports. For the study, in Neurology, researchers set up a controlled trial with 19,114 men and women older than 70 who were free of cardiovascular disease and dementia at the start. Half were randomly assigned to take a daily 100-milligram aspirin, while the other half took a placebo. After an average follow-up of almost five years with annual examinations, the researchers found no difference between the groups in diagnoses of Alzheimer’s disease or mild cognitive impairment. They did find declining cognitive function over time, but the speed and degree of that decline was the same in both groups. The researchers found no effect in various subgroups either — people with hypertension or diabetes, smokers or people with high cholesterol, or those who were overweight or obese. A limitation of the study was that patients were followed for less than five years. “If you’re 70 or older and healthy, without evidence of cardiovascular disease, it’s very difficult to improve on your success. The relatively low risk of dementia in this study was not further lowered with aspirin,” said a co-author, Dr. Anne B. Newman, a professor of epidemiology at the University of Pittsburgh. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27147 - Posted: 03.30.2020

By Julie Halpert As the coronavirus advances, it is taking a particularly harsh toll on the many who are caring for a loved one with dementia or Alzheimer’s, the most common form of dementia. According to a report by the Alzheimer’s Association, more than 16 million Americans are providing unpaid care for those with Alzheimer’s or other types of dementia. For them the virus is “really a double whammy,” said Lynn Friss Feinberg, a senior strategic policy adviser at AARP’s Public Policy Institute. “You’re worrying about your own health and that of your family member.” While the disease itself does not necessarily place patients at high risk for contracting the virus, they and their caregivers face a range of special challenges. Dementia patients are typically very sensitive to changes in routine and often require a great deal of hands-on care, both factors that are hard to manage now. Family members who usually rely on day care programs or visiting caregivers may be finding themselves with full-time responsibilities, while others whose loved ones are in facilities are unable to visit them now. Among the greatest challenges is how to minimize disruption in care that is intensely personal. “Care for dementia patients is ‘high touch,’” said Peter Lichtenberg, a professor of psychology and director of the Institute of Gerontology at Wayne State University. He recommends that caregivers take measures to avoid their own exposures by having provisions delivered, disinfecting surfaces and employing proper hand-washing techniques. K.C. Mehta has been caring for his wife, Sumi, since 2013, when she was given a diagnosis of Alzheimer’s at the age of 59. A former engineering executive at Chrysler, Mr. Mehta, who is 72 and lives in Rochester Hills, Mich., spends each day focused on maintaining his wife’s routine. Twice during the night, he changes her diaper. When she awakes, he bathes and dresses her. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27146 - Posted: 03.27.2020