By Christie Aschwanden In February, pharmaceutical companies Roche and Eli Lilly announced that two experimental drugs they had developed for Alzheimer’s disease had failed in clinical trials. Roche’s drug, gantenerumab, and Eli Lilly’s solanezumab joined more than 100 other potential Alzheimer’s drugs that have flopped, including aducanumab, a much-heralded drug from Biogen. In March 2019, Biogen announced that it had halted two clinical trials of the drug early after an interim analysis showed they weren’t working, but the company has since changed course, saying it intends to seek approval from the Food and Drug Administration based on a new analysis of the data. A lot is riding on Biogen's experimental drug. If approved, it "would be the first disease-modifying drug ever," says George Vradenburg, chairman and co-founder of the advocacy group UsAgainstAlzheimer's. The last time a drug was approved specifically for Alzheimer's was 2003, and since then, the Alzheimer's drug pipeline has spit out a bunch of duds. More than 200 promising leads have fallen through just in the past decade. There has been an ongoing search for Alzheimer's drugs since the 1990s, but "the long and short of it is that it's not been successful," says Lon Schneider, an Alzheimer's researcher at the University of Southern California's Keck School of Medicine. These failures aren’t for lack of trying. Instead, they are evidence that the disease and its causes are much more complex than researchers first appreciated. “We were blind to this [complexity]. Things looked simpler than they really are,” says Richard Hodes, director of the National Institute on Aging (NIA).

Keyword: Alzheimers
Link ID: 27172 - Posted: 04.06.2020

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 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

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

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

Richard Masland The eye is something like a camera, but there is a whole lot more to vision than that. One profound difference is that our vision, like the rest of our senses, is malleable and modifiable by experience. Take the commonplace observation that people deprived of one sense may have a compensatory increase in others — for example, that blind people have heightened senses of hearing and touch. A skeptic could say that this was just a matter of attention, concentration and practice at the task, rather than a true sensory improvement. Indeed, experiments show that a person’s sensory acuity can achieve major improvement with practice. Yet with modern methodologies, neuroscientists have conclusively proved that the circuits of the brain neurons do physically change. Our senses are malleable because the sensory centers of the brain rewire themselves to strike a useful balance between the capacities of the available neural resources and the demands put on them by incoming sensory impressions. Studies of this phenomenon are revealing that some sensory areas have innate tendencies toward certain functions, but they show just as powerfully the plasticity of the developing brain. Take a rat that has been deprived of vision since birth — let’s say because of damage to both retinas. When the rat grows up, you train that rat to run a maze. Then you damage the visual cortex slightly. You ask the rat to run the maze again and compare its time before the operation and after. In principle, damaging the visual cortex should not do anything to the maze-running ability of that blind rat. But the classic experimental finding made decades ago by Karl Lashley of Yerkes Laboratories of Primate Biology and others is that the rat’s performance gets worse, suggesting that the visual cortex in the blind rat was contributing something, although we do not know what it was.­­ All Rights Reserved © 2020

Keyword: Vision; Development of the Brain
Link ID: 27143 - Posted: 03.25.2020

Jordana Cepelewicz In the 1990s, an army of clones invaded Germany. Within a decade, they had spread to Italy, Croatia, Slovakia, Hungary, Sweden, France, Japan and Madagascar — wreaking havoc in rivers and lakes, rice paddies and swamps; in waters warm and cold, acidic and basic. The culprits: six-inch-long, lobster-like creatures called marbled crayfish. Scientists suspect that sometime around 1995, a genetic mutation allowed a pet crayfish to reproduce asexually, giving rise to a new, all-female species that could make clones of itself from its unfertilized eggs. Deliberately or accidentally, some of these mutants were released from aquariums into the wild, where they rapidly multiplied into the millions, threatening native waterways species and ecosystems. But their success is strange. “All marbled crayfish which exist today derive from a single animal,” said Günter Vogt, a biologist at Heidelberg University. “They are all genetically identical.” Ordinarily, the absence of genetic diversity makes a population exceedingly vulnerable to the vagaries of its environment. Yet the marbled crayfish have managed to thrive around the globe. A closer look reveals that the crayfishes’ uniformity is only genome-deep. According to studies conducted by Vogt and others in the mid-2000s, these aquatic clones actually vary quite a bit in their color, size, behavior and longevity. Which means that something other than their genes is inspiring that diversity. Common sense tells us that if it’s not nature, it’s nurture: environmental influences that interact with an animal’s genome to generate different outcomes for various traits. But that’s not the whole story. New research on crayfish and scores of other organisms is revealing an important role for a third, often-overlooked source of variation and diversity — a surprising foundation for what makes us unique that begins in the first days of an embryo’s development: random, intrinsic noise. All Rights Reserved © 2020

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27139 - Posted: 03.24.2020

By Amanda McCracken Over 30 years ago, Tom Johnson identified a gene that extended the very short life of a tiny roundworm, propelling him to the forefront of research on aging and raising the tantalizing possibility that aging could someday be slowed down in people, too. His work transformed the mind-set of scientists, launching a new field in the science of aging when he demonstrated that identifying and manipulating genes could lengthen life span. Although Johnson’s research has led to drug development to slow the effects of age-related diseases, he has yet to find the secret to stop aging. Now the soft-spoken redheaded scientist is running out of time as he confronts his own mortality. Five years ago, at age 66, work got confusing for Johnson, a professor in the Institute for Behavioral Genetics at the University of Colorado at Boulder. He found it impossible to keep track of his many projects. He began wondering whether he had Alzheimer’s like his newly diagnosed sister. He spoke to his wife, Vicki Simpson, about the little dogs he frequently saw running around the house (even though he knew they weren’t real). Simpson, a retired anesthesiologist, later learned such hallucinations are a trademark sign of Lewy body dementia. At first, she praised his imagination and then after several months suggested they visit a memory clinic. There he was diagnosed with probable Lewy body — a fatal disease with inescapable dementia that can be diagnosed with certainty only at death. Right now, there is no cure, only ways to ease symptoms.

Keyword: Alzheimers; Genes & Behavior
Link ID: 27134 - Posted: 03.23.2020

Peter Hess The coronavirus pandemic has shuttered universities and institutes, leaving scientists scrambling to continue their research. Hundreds of colleges and universities in the United States have dispatched students home and are aiming to transition to remote learning. Scientific organizations are canceling conferences or moving them online. And scientists have had to put research projects and clinical trials on hold. These decisions—all done with the intention of slowing the pandemic—may stall and stymie research, with long-term consequences for the field. It may also hurt career prospects for graduate students who rely on conference presentations to gain exposure. “From everything that we’re seeing, this isn’t like a two-week hiatus,” says Helen Egger, chair of the child and adolescent psychiatry department at NYU Langone Health in New York City. “We’re in the middle of the hurricane, and there’s no indication how much worse it’s going to get or when it will end.” One long-term benefit is that the crisis may give universities and professional organizations a crash course in embracing technology. “These types of experiences—as long as we are having them, unfortunately—are giving autism [researchers] and other researchers more skills to be able to have online conferences and online teaching as needed,” says Steven Kapp, lecturer in psychology at the University of Portsmouth in the United Kingdom. Backup plans: Some labs were prepared to meet the challenge, and they quickly put their emergency plans into place when news of the pandemic intensified. But, illustrating how rapidly the situation is changing, some of their plans derailed over the weekend. © 1986–2020 The Scientist

Keyword: Autism
Link ID: 27132 - Posted: 03.21.2020

May-Britt Moser & Edvard Moser There was something of the Viking about Per Andersen. The intrepid and steadfast Norwegian was renowned for his attacks on the deepest puzzle of the brain: how its wiring and electrical activity give rise to behaviour and experience. When he was a student in the 1950s, most neuroscientists studied accessible parts of the mammalian nervous system — the junctions between nerves and muscles, say. Andersen worked on the cerebral cortex, which processes higher-level functions: perception, voluntary movement, planning and abstract thinking. His pioneering recordings of electrical activity in the hippocampus — a part of the cortex involved in memory — launched a new era in physiological understanding of the brain and laid the foundations of modern systems neuroscience. He died on 17 February, aged 90. In 1949, it was predicted that learning might depend on repeated activity strengthening the connections — synapses — in networks of neurons. Andersen saw that this was the case in the hippocampus. As the effect was too fleeting to account directly for memory storage, he encouraged his student Terje Lømo to investigate. In 1973, in one of the greatest discoveries of twentieth-century neuroscience, Lømo and British visiting scholar Tim Bliss reported from Andersen’s laboratory that many bursts of electrical stimulation at certain frequencies enhanced connectivity for hours or days. This phenomenon — long-term potentiation (LTP) — remains the main explanation for how we form and store memories (T. V. P. Bliss and T. Lømo J. Physiol. 232, 331–356; 1973). We met Andersen as students, in the late 1980s. Our work with him on LTP and animal learning found differences in function between regions of the hippocampus and demonstrated changes in connectivity related to behaviour. His hunch that we should record activity from single cells led to our discovery of specialized neurons in the cortex that support the sense of where the body is in space. The work was a direct result of his insight. © 2020 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 27130 - Posted: 03.21.2020

By Adrienne Raphel Let me tell you a tale of two grandfathers, Irv and Murray. For decades, Irv, an introverted, quiet, retired bartender and former military engineer, had the same morning routine: coffee and cream; a roll; and the puzzle page of the Press of Atlantic City. He methodically and religiously worked his way through each one, from the crossword to the jumble to the cryptoquip, a substitution cipher that asks solvers to decode clues and figure out the pun. Extroverted and spontaneous Murray, a successful businessman and local politician, also had his morning routine: coffee with lots of sugar; oatmeal; and tinkering on one of his many writing projects, such as a loosely autobiographical musical about a traveling salesman. Murray swam a few times a week, devoured books and loved to travel. But he never did crosswords. Irv died at age 94, and he barely experienced any cognitive loss before the last six months of his life, when he exhibited rapid mental decline. Murray lived to be 91, but the last several years of his life were marked with severe dementia. When I was researching my book Thinking Inside the Box: Adventures with Crosswords and the Puzzling People Who Can’t Live Without Them, I was fascinated by my family’s case study. The evidence, it seemed, couldn’t be clearer: doing crosswords late in life prevents dementia. And at first, all the studies I found seemed to bear this hypothesis out. “Regular crosswords and number puzzles linked to sharper brain in later life,” a May 2019 Science Daily headline proclaims. According to a University of Exeter study, older adults who regularly did word and number puzzles had increased mental acuity. A 2011 experiment with members of the Bronx Aging Study found that a regular regimen of crosswords might delay the onset of cognitive decline. Belief in puzzle power has fueled multimillion-dollar industry of brain-training games like Lumosity or Dakim. © 2020 Scientific American,

Keyword: Alzheimers; Learning & Memory
Link ID: 27124 - Posted: 03.17.2020

By Linda Searing Alzheimer’s disease, the most common dementia among older adults, now affects about 5.8 million U.S. residents 65 and older — 10 percent of that age group, according to a new report from the Alzheimer’s Association. Age is considered the biggest risk factor for Alzheimer’s, with 3 percent of people 65 to 74, 17 percent of those 75 to 84 and 32 percent of people 85 and older — or nearly a third — having the disease. By 2050, the number of U.S. adults 65 and older with Alzheimer’s is expected to reach 13.8 million, with about half of them 85 or older. The association’s report attributes the growing number of Americans with Alzheimer’s to the projected aging of the U.S. population, with the West and Southeast regions of the country expected to experience the largest increases in the next five years. Sometimes, people under 65 develop what is called early-onset Alzheimer’s, but that is much less common. Although there is no known average age for the onset of Alzheimer’s, symptoms tend to be noticeable in the mid-60s, with memory issues typically one of the first signs. Alzheimer’s is an irreversible brain disorder that slowly destroys memory and thinking skills, can alter mood and personality and eventually disrupts the ability to carry out simple day-to-day tasks. Hallucinations, agitation and aggression are common symptoms as the condition advances. Although there is no cure for the disease — or even drugs to slow or stop progression — some medications can temporarily improve cognitive or behavioral symptoms. Non-medication therapies — exercise, music to stir recall or special lighting to ease sleep disorders — also can be helpful, but the report says that they also do not stop or slow the disease.

Keyword: Alzheimers
Link ID: 27123 - Posted: 03.17.2020

By Scott Barry Kaufman For many years, researchers have treated the individual traits and characteristics of autistic people as an enduring essence of their autism-- in isolation of the social context and without even asking autistic people what their social life is actually like. However, perspective matters. Who is to say it's autistic people who are the "awkward" ones? A number of myths about autistic people abound. For one, it's a great myth that autistic people lack empathy. This is how they were depicted for so many years in the clinical literature and in the media-- as emotionless, socially clueless robots. However, the more you get to know an autistic person, the more you realize just how caring they can be, even though they may have some difficulties reading social cues. As Steve Silberman points out, empathy is a two-way street. Another common misconception is that autistic people aren't social. I really like some recent approaches that add greater complexity to this issue, showing that when you take a contextual strengths-based approach you can see that people on the autism spectrum are much more social than researchers ever realized. The lens upon which we look at a person matters. As Megan Clark and Dawn Adams put it, "When autism is viewed through a deficit lens the strengths, positive attributes and interests of individuals on the spectrum can be overshadowed." In one recent study, Clark and Adams asked 83 children on the autism spectrum (aged 8 to 15 years) various questions about themselves. When asked "What do you like most about yourself?", the most common themes were "I am a good friend or person to be around" and "I am good at particular things."When asked "What do you enjoy the most?", one of the most endorsed themes was social interaction. © 2020 Scientific American

Keyword: Autism
Link ID: 27121 - Posted: 03.16.2020

Joanna Moorhead For artist and writer Charlotte Amelia Poe, 30, every day feels like a walk across a frozen pond. “It’s how it’s always been,” she explains. “You’re trying to navigate it and stay safe, but you’re aware that at any moment the ice is likely to crack, and at that point you will sink into the water.” The worst of it is that, when she feels that way, she has no idea how she can avoid going under. “You think you’re doing fine and you’re treading carefully enough not to crack the ice. But suddenly you’ve gone under. You’ve got it completely wrong – and you’ve no idea why.” Poe is describing how it feels to be autistic. She wants the rest of us to understand, she says, because it really matters, perhaps more than it’s ever mattered (of which more later). Her mission to break open the mystery of how it feels to be autistic has already been impressively successful: last year she won the Spectrum art prize for her video piece How To Be Autistic and recently she wrote a book of the same name. Her hope is that, by opening up about her own journey through childhood, school and adolescence, she can change other people’s perceptions and expectations about what autism is like, from the inside. We are talking in the sitting room of the semi-detached house overlooking a Suffolk field that Poe shares with three generations of her family. She has never left home and doesn’t expect to; her nephews and niece are playing outside in the garden, and one day their mother, her sister, will be her carer in the way that her parents are at the moment. © 2020 Guardian News & Media Limited

Keyword: Autism
Link ID: 27120 - Posted: 03.16.2020

By Judson A. Brewer, M.D. Anxiety is a strange beast. As a psychiatrist, I have learned that anxiety and its close cousin, panic, are both born from fear. As a behavioral neuroscientist, I know that fear’s main evolutionary function is helping us survive. In fact, fear is the oldest survival mechanism we have. Fear helps us learn to avoid dangerous situations in the future through a process called negative reinforcement. For example, if we step out into a busy street, turn our head and see a car coming right at us, we instinctively jump back onto the safety of the sidewalk. Evolution made this really simple for us. So simple that we only need three elements in situations like this to learn: an environmental cue, a behavior and a result. In this case, walking up to a busy street cues us to look both ways before crossing. The result of not getting killed helps us remember to repeat the action again in the future. Sometime in the last million years, humans evolved a new layer on top of our more primitive survival brain, called the prefrontal cortex. Involved in creativity and planning, the prefrontal cortex helps us think and plan for the future. It predicts what will happen in the future based on past experience. If information is lacking, our prefrontal cortex lays out different scenarios about what might happen, and guesses which will be most likely. It does this by running simulations based on previous events that are most similar. Defined as “a feeling of worry, nervousness or unease, typically about an imminent event or something with an uncertain outcome,” anxiety comes up when our prefrontal cortexes don’t have enough information to accurately predict the future. We see this right now with coronavirus. Without accurate information, it is easy for our brains to spin stories of fear and dread. © 2020 The New York Times Company

Keyword: Emotions; Stress
Link ID: 27117 - Posted: 03.14.2020

As we get older, we become more easily distracted, but it isn't always a disadvantage, according to researchers. Tarek Amer, a psychology postdoctoral research fellow at Columbia University, says that although our ability to focus our attention on specific things worsens as we get older, our ability to take in broad swaths of information remains strong. So in general, older adults are able to retain information that a more focused person could not. For the last few years, Amer's research has focused mainly on cognitive control, a loose term that describes one's ability to focus their attention. His work at the University of Toronto, where he received his PhD in 2018, looked specifically at older adults aged 60 to 80. Amer joined Spark host Nora Young to discuss his research and how it could be implemented in practical ways. What happens to our ability to concentrate as we get older? There's a lot of research that shows as we get older, this ability tends to decline or is reduced with age. So essentially, what we see is that relative to younger adults, older adults have a harder time focusing on one thing while ignoring distractions. This distraction can be from the external world. This can also be internally based distractions, such as our own thoughts, which are usually not related to the task at hand. With respect to mind wandering specifically, the literature is ... mixed. [The] typical finding is that older adults tend to, at least in lab-based tasks, mind wander less. So I know that you've been looking, in your own research, at concentration and memory formation. So what exactly are you studying? One of the things I was interested in is whether this [decline in the ability to concentrate] could be associated with any benefits in old age. For example, one thing that we showed is that when older and younger adults perform a task that includes both task-relevant as well as task-irrelevant information, older adults are actually processing both types of information. So if we give them a memory task at the end that actually is testing memory for the irrelevant information … we see that older adults actually outperform younger adults. ©2020 CBC/Radio-Canada.

Keyword: Attention; Alzheimers
Link ID: 27116 - Posted: 03.14.2020

By R. Douglas Fields Our concepts of how the two and a half pounds of flabby flesh between our ears accomplish learning date to Ivan Pavlov’s classic experiments, where he found that dogs could learn to salivate at the sound of a bell. In 1949 psychologist Donald Hebb adapted Pavlov’s “associative learning rule” to explain how brain cells might acquire knowledge. Hebb proposed that when two neurons fire together, sending off impulses simultaneously, the connections between them—the synapses—grow stronger. When this happens, learning has taken place. In the dogs’ case, it would mean the brain now knows that the sound of a bell is followed immediately by the presence of food. This idea gave rise to an oft-quoted axiom: “Synapses that fire together wire together.” The theory proved sound, and the molecular details of how synapses change during learning have been described in detail. But not everything we remember results from reward or punishment, and in fact, most experiences are forgotten. Even when synapses do fire together, they sometimes do not wire together. What we retain depends on our emotional response to an experience, how novel it is, where and when the event occurred, our level of attention and motivation during the event, and we process these thoughts and feelings while asleep. A narrow focus on the synapse has given us a mere stick-figure conception of how learning and the memories it engenders work. It turns out that strengthening a synapse cannot produce a memory on its own, except for the most elementary reflexes in simple circuits. Vast changes throughout the expanse of the brain are necessary to create a coherent memory. Whether you are recalling last night’s conversation with dinner guests or using an acquired skill such as riding a bike, the activity of millions of neurons in many different regions of your brain must become linked to produce a coherent memory that interweaves emotions, sights, sounds, smells, event sequences and other stored experiences. Because learning encompasses so many elements of our experiences, it must incorporate different cellular mechanisms beyond the changes that occur in synapses. This recognition has led to a search for new ways to understand how information is transmitted, processed and stored in the brain to bring about learning. In the past 10 years neuroscientists have come to realize that the iconic “gray matter” that makes up the brain’s outer surface—familiar from graphic illustrations found everywhere, from textbooks to children’s cartoons—is not the only part of the organ involved in the inscription of a permanent record of facts and events for later recall and replay. It turns out that areas below the deeply folded, gray-colored surface also play a pivotal role in learning. © 2020 Scientific American

Keyword: Learning & Memory; Glia
Link ID: 27114 - Posted: 03.12.2020