Chapter 13. Memory and Learning

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By Nicholas Bakalar Severe gum disease and tooth loss may be linked to an increased risk for developing dementia, a new study has found. Researchers looked at 8,275 men and women whose average age was 63 at the start of the study. Over an average follow-up of more than 18 years, 19 percent of them developed Alzheimer’s disease or other forms of dementia. After controlling for various characteristics, including age, sex, education, cholesterol, high blood pressure, coronary heart disease, smoking and body mass index, they found that compared with people with healthy gums, those who had severe gingivitis with tooth loss had a 22 percent increased relative risk for dementia. Being toothless was associated with a 26 percent increased risk. The report is in the journal Neurology. Previous studies have shown that bacteria present in periodontal disease, particularly certain spirochetes, can travel along the trigeminal nerve that connects the mucous membranes of the mouth to the brain, potentially causing brain damage. The researchers also suggest that the connection could be more indirect, with the inflammation of gum disease leading to cardiovascular disease or diabetes, which are known risk factors for dementia. “We haven’t proven causation,” said the lead author, Ryan T. Demmer, an associate professor of epidemiology at the University of Minnesota. “But if it is causal, the population impact could be significant. Half the population has periodontal disease severe enough to put them at higher risk.” © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27392 - Posted: 07.31.2020

By Pam Belluck A newly developed blood test for Alzheimer’s has diagnosed the disease as accurately as methods that are far more expensive or invasive, scientists reported on Tuesday, a significant step toward a longtime goal for patients, doctors and dementia researchers. The test has the potential to make diagnosis simpler, more affordable and widely available. The test determined whether people with dementia had Alzheimer’s instead of another condition. And it identified signs of the degenerative, deadly disease 20 years before memory and thinking problems were expected in people with a genetic mutation that causes Alzheimer’s, according to research published in JAMA and presented at the Alzheimer’s Association International Conference. Such a test could be available for clinical use in as little as two to three years, the researchers and other experts estimated, providing a readily accessible way to diagnose whether people with cognitive issues were experiencing Alzheimer’s, rather than another type of dementia that might require different treatment or have a different prognosis. A blood test like this might also eventually be used to predict whether someone with no symptoms would develop Alzheimer’s. “This blood test very, very accurately predicts who’s got Alzheimer’s disease in their brain, including people who seem to be normal,” said Dr. Michael Weiner, an Alzheimer’s disease researcher at the University of California, San Francisco, who was not involved in the study. “It’s not a cure, it’s not a treatment, but you can’t treat the disease without being able to diagnose it. And accurate, low-cost diagnosis is really exciting, so it’s a breakthrough.” Nearly six million people in the United States and roughly 30 million worldwide have Alzheimer’s, and their ranks are expected to more than double by 2050 as the population ages. Blood tests for Alzheimer’s, which are being developed by several research teams, would provide some hope in a field that has experienced failure after failure in its search for ways to treat and prevent a devastating disease that robs people of their memories and ability to function independently. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27388 - Posted: 07.29.2020

Jon Hamilton This is the story of a fatal genetic disease, a tenacious scientist and a family that never lost hope. Conner Curran was 4 years old when he was diagnosed with Duchenne Muscular Dystrophy, a genetic disease that causes muscles to waste away. Conner's mother, Jessica Curran, remembers some advice she got from the doctor who made that 2015 diagnosis: "Take your son home, love him, take him on trips while he's walking, give him a good life and enjoy him because there are really not many options right now." Five years later, Conner is not just walking, but running faster than ever, thanks to an experimental gene therapy that took more than 30 years to develop. Conner was the first child to receive the treatment — a single infusion designed to fix the genetic mutation that was gradually causing his muscles cells to die. The treatment can't bring back the cells he's lost (he remains smaller and weaker than his twin brother, Kyle), but it has allowed the muscle cells he still has to function better. Since Conner's treatment, eight other boys with Duchenne have received two different doses of the gene therapy. Preliminary results on six of them, tested a year after treatment, showed they, too, had improved strength and endurance at an age when boys with Duchenne usually become weaker. © 2020 npr

Keyword: Muscles; Movement Disorders
Link ID: 27387 - Posted: 07.27.2020

Jon Hamilton For years, public health officials have been trying to dispel the myth that people who get a flu shot are more likely to get Alzheimer's disease. They are not. And now there is evidence that vaccines that protect against the flu and pneumonia may actually protect people from Alzheimer's, too. The evidence comes from two studies presented Monday at this year's Alzheimer's Association International Conference, which is being held as a virtual event. "We've always known that vaccines are very important to our overall health," says Maria Carrillo, chief science officer of the Alzheimer's Association. "And maybe they even contribute to protecting our memory, our cognition, our brain." The first study came from a team at the University of Texas that combed through millions of medical records in a national database. The goal was to find factors that affected a person's risk of getting certain diseases, including Alzheimer's. "And one of the things that came back was flu shots," says Albert Amran, a medical student of the McGovern Medical School at the University of Texas Health Science Center in Houston and an author of the study. That seemed odd. So Amran and a team of researchers took a closer look at the medical records of about 9,000 people who were at least 60 years old. Some had received a seasonal flu shot. Some hadn't. "We [tried] to make sure that both groups had an equal amount of, say, smoking status, obesity, diabetes, cardiovascular disease," Amran says. Those are known risk factors for Alzheimer's. The team also looked at factors like education and income, and indicators like the number of prescriptions a person had received, to make sure that people who got vaccines weren't just healthier overall. They weren't. © 2020 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 27385 - Posted: 07.27.2020

by Peter Hess / Infants with particular patterns of electrical activity in the brain go on to have high levels of autism traits as toddlers, a new study shows1. Specifically, babies who have unusually high or low synchrony between certain brain waves — as measured by electroencephalography (EEG) — at 3 months old tend to score high on a standardized scale of autism-linked behaviors when they are 18 months old. These levels of synchrony reflect underlying patterns of connectivity in the brain. The findings suggest that EEG could help clinicians identify autistic babies long before these children show behaviors flagged by standard diagnostic tests. The work “reinforces the concept and the truism that brain development is affected before autism diagnoses are made,” says lead researcher Shafali Spurling Jeste, associate professor of psychiatry and neurology at the University of California, Los Angeles. “We believe that we could work to start rewiring the brain if we intervene effectively and early enough. That message, quite simply, is a very important one.” The study involved ‘baby sibs,’ the younger siblings of autistic children. Baby sibs are 10 to 20 times more likely to have autism than the general population. Previous research showed similar patterns of altered connectivity in functional magnetic resonance imaging (MRI) data from infants who were later diagnosed with autism, but MRI is costly and prone to errors. EEG measurements, on the other hand, are relatively inexpensive and simple to perform, which makes them more practical for clinical use, says Charles Nelson, professor of pediatrics and neuroscience at Harvard University, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27380 - Posted: 07.25.2020

A scientific analysis of more than 2,000 brain scans found evidence for highly reproducible sex differences in the volume of certain regions in the human brain. This pattern of sex-based differences in brain volume corresponds with patterns of sex-chromosome gene expression observed in postmortem samples from the brain’s cortex, suggesting that sex chromosomes may play a role in the development or maintenance of sex differences in brain anatomy. The study, led by researchers at the National Institute of Mental Health (NIMH), part of the National Institutes of Health, is published in Proceedings of the National Academy of Sciences. “Developing a clearer understanding of sex differences in human brain organization has great importance for how we think about well-established sex differences in cognition, behavior, and risk for psychiatric illness. We were inspired by new findings on sex differences in animal models and wanted to try to close the gap between these animal data and our models of sex differences in the human brain,” said Armin Raznahan, M.D., Ph.D., study co-author and chief of the NIMH Section on Developmental Neurogenomics. Researchers have long observed consistent sex-based differences in subcortical brain structures in mice. Some studies have suggested these anatomical differences are largely due to the effects of sex hormones, lending weight to a “gonad-centric” explanation for sex-based differences in brain development. However, more recent mouse studies have revealed consistent sex differences in cortical structures, as well, and gene-expression data suggest that sex chromosomes may play a role in shaping these anatomical sex differences. Although the mouse brain shares many similarities with the human brain, it is not clear whether these key findings in mice also apply to humans.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 27377 - Posted: 07.21.2020

by Angie Voyles Askham The autism gene SHANK3 is crucial for the development and function of muscles and the motor neurons that control them, according to a new study1. This relationship may explain why some people with mutations in the gene have low muscle tone, says co-lead investigator Maria Demestre, senior researcher at the Institute for Bioengineering of Catalonia in Barcelona. “It opens an avenue for treatment.” Between 1 and 2 percent of people with autism have a mutation in SHANK3. Deletions of the chromosomal region containing SHANK3 lead to Phelan-McDermid syndrome, characterized by intellectual disability, speech delay and, often, autism. One of the earliest signs of the syndrome in infants is hypotonia, or low muscle tone, which can result in difficulty feeding and a delay in reaching developmental milestones such as crawling and walking. SHANK3 encodes a protein that helps neurons communicate throughout the brain. But studies have shown that the gene is also found in other parts of the body and that mutations or deletions of genes in peripheral cells can contribute to autism traits2. SHANK3 is heavily expressed throughout the motor system of both mice and people, the new work shows. Muscle cells derived from people with Phelan-McDermid syndrome fail to mature, and mice deficient in SHANK3 have poor muscle function. The results add to “the growing appreciation of the role of autism-associated genes — in this case, SHANK3 — outside of the brain,” says David Ginty, professor of neurobiology at Harvard Medical School, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 27375 - Posted: 07.21.2020

by Jonathan Moens / Autistic people with deletions in the chromosomal region 22q11.2 have a brain structure that’s distinct from that of autistic people without the deletions, according to a new brain imaging study1. The findings suggest that brain changes related to autism vary depending on the condition’s etiology, says study investigator Carrie Bearden, professor of clinical psychology at the University of California, Los Angeles. “[Autism is] really not one thing.” Deletions in 22q11.2 cause a syndrome characterized by heart defects, learning difficulties and an increased risk of psychiatric conditions such as schizophrenia. About 16 percent of people with the syndrome have autism2. Brain anatomy differs between people with the syndrome who have autism and those who do not, past studies by the same team show3. The new work is the first to compare these two groups with people who have ‘idiopathic’ autism, meaning its etiology is unknown. Disentangling these brain differences may be key to understanding if clinicians should treat autistic people with 22q deletions differently than people with autism without the deletions, Bearden says. “Maybe we’re treating these [conditions] as all the same at one level when we really need to dissect this a bit more.” Some experts say these findings could also be a first step toward dividing autism’s broad spectrum of traits into smaller sets of genetic conditions. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27372 - Posted: 07.18.2020

Ian Sample Science editor Doctors in France have reported what they believe to be the first proven case of Covid-19 being passed on from a pregnant woman to her baby in the womb. The newborn boy developed inflammation in the brain within days of being born, a condition brought on after the virus crossed the placenta and established an infection prior to birth. He has since made a good recovery. The case study, published in Nature Communications, follows the birth of a number of babies with Covid-19 who doctors suspect contracted the virus in the womb. Until now, they have not been able to rule out the possibility that the babies were infected during or soon after delivery. “Unfortunately there is no doubt about the transmission in this case,” said Daniele De Luca, medical director of paediatrics and neonatal critical care at the Antoine Béclère hospital in Paris. “Clinicians must be aware that this may happen. It’s not common, that’s for sure, but it may happen and it must be considered in the clinical workout.” The 23-year-old mother was admitted to the hospital on 24 March with a fever and severe cough after contracting coronavirus late in the third trimester. She tested positive for Covid-19 shortly her arrival. Three days after the woman was admitted, monitoring of the baby revealed signs of distress and doctors performed an emergency caesarean with the mother under general anaesthetic. The baby was immediately isolated in a neonatal intensive care unit and intubated because he was affected by the general anaesthetic. © 2020 Guardian News & Media Limited

Keyword: Development of the Brain
Link ID: 27366 - Posted: 07.15.2020

by Sarah DeWeerdt The amygdala is a deep brain structure about the size and shape of an almond — from which it gets its name. It is commonly described as a center for detecting threats in the environment and for processing fear and other emotions. Researchers who study the region argue that its function is broader — and that it plays a crucial role in autism. “Emotion is such a big part in social function,” says Wei Gao, associate professor of biomedical sciences at Cedars-Sinai Medical Center in Los Angeles, California. “So I think the amygdala has got to have a big role in the emergence or development of autism-related traits.” The amygdala is the brain’s surveillance hub: involved in recognizing when someone with an angry face and hostile body language gets closer, tamping down alarm when a honeybee buzzes past, and paying attention when your mother teaches you how to cross the street safely and points out which direction traffic will be coming from — in other words, things people should run away from, but also those they should look toward, attend to and remember. In that sense, researchers say, this little knot of brain tissue shows just how tangled up emotion and social behavior are for humans. “Important events tend to be emotional in nature,” as do most aspects of social behavior, says John Herrington, assistant professor of psychiatry at the Children’s Hospital of Philadelphia in Pennsylvania. As a result, the amygdala has long been a focus of autism research, but its exact role in the condition is still unclear. © 2020 Simons Foundation

Keyword: Autism; Emotions
Link ID: 27363 - Posted: 07.15.2020

By Nicholas Bakalar Artificial outdoor light at night may disrupt adolescents’ sleep and raise the risk for psychiatric disorders, a new study suggests. Researchers tracked the intensity of outdoor light in representative urban and rural areas across the country using satellite data from the National Oceanic and Atmospheric Administration. They interviewed more than 10,123 adolescents living in these neighborhoods about their sleep patterns, and assessed mental disorders using well-validated structured scales. They also interviewed the parents of more than 6,000 of the teenagers about their children. The study, in JAMA Psychiatry, found that the more intense the lighting in your neighborhood, the more sleep was disrupted and the greater the risk for depression and anxiety. After adjustment for other factors such as sex, race, parental education and population density, they found that compared with the teenagers in the one-quarter of neighborhoods with the lowest levels of outdoor light, those in the highest went to bed, on average, 29 minutes later and reported 11 fewer minutes of sleep. Adolescents living in the most intensely lit neighborhoods had a 19 percent increased risk for bipolar illness, and a 7 percent increased risk for depression. The study is observational, and does not prove cause and effect. The senior author, Kathleen R. Merikangas, a senior investigator with the National Institute of Mental Health, said that future policy changes could make a difference. In the meantime, she said, “At least as individuals, we ought to try to minimize exposure to light at night.” © 2020 The New York Times Company

Keyword: Sleep; Biological Rhythms
Link ID: 27362 - Posted: 07.15.2020

For every cell in the body there comes a time when it must decide what it wants to do for the rest of its life. In an article published in the journal PNAS, National Institutes of Health researchers report for the first time that ancient viral genes that were once considered “junk DNA” may play a role in this process. The article describes a series of preclinical experiments that showed how some human endogenous retrovirus (HERV-K) genes inscribed into chromosomes 12 and 19 may help control the differentiation, or maturation, of human stem cells into the trillions of neurons that are wired into our nervous systems. The experiments were performed by researchers in a lab led by Avindra Nath, M.D., clinical director, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Over the course of evolution, the human genome has absorbed thousands of human endogenous retrovirus genes. As a result, nearly eight percent of the DNA that lines our chromosomes includes remnants of these genes. Although once thought to be inactive, or “junk”, recent studies have shown that these genes may be involved in human embryonic development, the growth of some tumors, and nerve damage during multiple sclerosis. Previously, researchers in Dr. Nath’s lab showed that amyotrophic lateral sclerosis (ALS) may be linked to activation of the HERV-K gene. In this study, led by Tongguang (David) Wang, M.D., Ph.D., staff scientist at NINDS, the team showed that deactivation of the gene may free stem cells to become neurons. The researchers performed most of their experiments on blood cells, drawn from healthy volunteers at the NIH’s Clinical Center, that they genetically transformed into induced pluripotent stem cells, which can then turn into any cell type in the body. Surprisingly, they found that the surfaces of the stem cells were lined with high levels of HERV-K, subtype HML-2, an envelope protein, that viruses often use to latch onto and infect cells. These proteins progressively disappeared as the cells were served two rounds of “cocktails.” One round nudged the cells into an intermediate, neural stem cell state followed by a second round that pushed the cells into finally becoming neurons.

Keyword: ALS-Lou Gehrig's Disease ; Development of the Brain
Link ID: 27359 - Posted: 07.14.2020

By Laura Sanders Exercise’s power to boost the brain might require a little help from the liver. A chemical signal from the liver, triggered by exercise, helps elderly mice keep their brains sharp, suggests a study published in the July 10 Science. Understanding this liver-to-brain signal may help scientists develop a drug that benefits the brain the way exercise does. Lots of studies have shown that exercise helps the brain, buffering the memory declines that come with old age, for instance. Scientists have long sought an “exercise pill” that could be useful for elderly people too frail to work out or for whom exercise is otherwise risky. “Can we somehow get people who can’t exercise to have the same benefits?” asks Saul Villeda, a neuroscientist at the University of California, San Francisco. Villeda and colleagues took an approach similar to experiments that revealed the rejuvenating effects of blood from young mice (SN: 5/5/14). But instead of youthfulness, the researchers focused on fitness. The researchers injected sedentary elderly mice with plasma from elderly mice that had voluntarily run on wheels over the course of six weeks. After eight injections over 24 days, the sedentary elderly mice performed better on memory tasks, such as remembering where a hidden platform was in a pool of water, than elderly mice that received injections from sedentary mice. Comparing the plasma of exercised mice with that of sedentary mice showed an abundance of proteins produced by the liver in mice that ran on wheels. The researchers closely studied one of these liver proteins produced in response to exercise, called GPLD1. GPLD1 is an enzyme, a type of molecular scissors. It snips other proteins off the outsides of cells, releasing those proteins to go do other jobs. Targeting these biological jobs with a molecule that behaves like GPLD1 might be a way to mimic the brain benefits of exercise, the researchers suspect. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Development of the Brain
Link ID: 27358 - Posted: 07.11.2020

By Jocelyn Kaiser It’s well established that exercise can sharpen the mind: People and mice who work out do better on cognitive tests, and elderly people who are physically active reduce their risk of dementia. Now, in a surprising finding, researchers report that blood from a mouse that exercises regularly can perk up the brain of a “couch potato” mouse. This effect, traced to a specific liver protein in the blood, could point the way to a drug that confers the brain benefits of exercise to an old or feeble person who rarely leaves a chair or bed. “Can your brain think that you exercised, from just something in your blood?” asks aging researcher Saul Villeda of the University of California, San Francisco (UCSF), who led the rodent research. The study grew out of research in Villeda’s lab and others suggesting blood from a young mouse can rejuvenate the brain and muscles of an old mouse. Some teams have since claimed to find specific proteins that explain the benefits of this “young blood.” Graduate student Alana Horowitz and postdoc Xuelai Fan in Villeda’s group wondered whether exercise—not just youth—could confer similar benefits via the blood. It was easy to enough to test: Put a wheel in a cage full of mice, and the mostly inactive animals will run for miles at night. The researchers collected blood from elderly or middle-aged mice that had an exercise wheel in their cage for 6 weeks and then transfused this blood into old mice without a wheel in their cage. Couch potato mice receiving this blood eight times over 3 weeks did nearly as well on learning and memory tests, such as navigating through a maze, as the exercising mice. A control group of couch potatoes receiving blood from similarly old, nonexercising mice saw no boost. The rodents getting the blood from the active mice also grew roughly twice as many new neurons in the hippocampus, a brain region involved in learning and memory, Villeda’s team reports today in Science. That change is comparable to what’s seen in rodents that directly exercise. © 2020 American Association for the Advancement of Science.

Keyword: Alzheimers; Development of the Brain
Link ID: 27357 - Posted: 07.11.2020

by Angie Voyles Askham An experimental drug prevents seizures and improves memory in a mouse model of fragile X syndrome, according to a new study1. The drug selectively blocks an enzyme that is overactive in the brains of people with fragile X and could offer a potential treatment for the condition. “It’s truly a novel target,” says co-lead investigator Mark Bear, professor of neuroscience at the Massachusetts Institute of Technology. Fragile X syndrome is characterized by intellectual disability, seizures, hyperactivity and, in one out of three people, autism. It results from mutations that diminish the gene FMR1’s production of FMRP, a protein that limits the synthesis of other proteins at synapses, where neurons exchange chemical messages. Without FMRP, according to one leading theory, proteins build up at synapses and disrupt this signaling, leading to fragile X’s outward signs. The new drug helps put the brakes on protein buildup by blocking a specific form of an enzyme called glycogen synthase kinase 3 (GSK3), which plays an important role during brain development. Previous trials have prevented protein buildup by blocking a different target, the mGluR5 receptor, which helps control protein production in neurons. But those drugs have failed in clinical trials because people have experienced adverse side effects and built up a tolerance to chronic dosing. The drug to block GSK3, called BRD0705, may result in fewer side effects because it is highly selective. The enzyme comes in two forms, known as alpha and beta, and BRD0705 blocks only the former. The findings should stimulate more research on GSK3 alpha, which has not been studied as well as its counterpart, researchers say. © 2020 Simons Foundation

Keyword: Development of the Brain
Link ID: 27355 - Posted: 07.11.2020

Jon Hamilton The same process that causes dew drops to form on a blade of grass appears to play an important role in Alzheimer's disease and other brain diseases. The process, known as phase transition, is what allows water vapor to condense into liquid water, or even freeze into solid ice. That same sort of process allows brain cells to constantly reorganize their inner machinery. But in degenerative diseases that include amyotrophic lateral sclerosis, frontotemporal dementia and Alzheimer's, the phase transitions inside neurons seem to go awry, says Dr. J. Paul Taylor, a neurogeneticist at St. Jude Children's Research Hospital in Memphis, and an investigator with the Howard Hughes Medical Institute. This malfunctioning prompts the interior of the cell to become too viscous, Taylor says. "It's as if you took a jar of honey [and] left it in the refrigerator overnight." In this sticky environment, structures that previously could nimbly disassemble and move around become "irreversibly glommed together," says Clifford Brangwynne, a professor of chemical and biological engineering at Princeton University and an investigator with the Howard Hughes Medical Institute. "And when they're irreversibly stuck like that, they can no longer leave to perform functions elsewhere in the cell." That glitch seems to allow toxins to begin to build up in and around these dysfunctional cells, Taylor says — including the toxins associated with Alzheimer's and other neurodegenerative diseases. The science behind this view of brain diseases has emerged only in the past decade. In 2009, Brangwynne was part of a team that published a study showing that phase transitions are important inside cells — or at least inside the reproductive cells of worms. © 2020 npr

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 27351 - Posted: 07.08.2020

by Angie Voyles Askham Toddlers with autism have unusually strong connections between sensory areas of the brain, according to a new study1. And the stronger the connections, the more pronounced a child’s autism traits tend to be. Overconnectivity in sensory areas may get in the way of an autistic child’s brain development, says lead investigator Inna Fishman, associate research professor at San Diego State University in California. “Their brain is busy with things it shouldn’t be busy with.” The findings add to a complicated field of research on brain connectivity and autism, which has shown weakened connectivity between some brain areas, strengthened connectivity between others, or no difference in connectivity at all. Previous brain-imaging studies have found that babies and toddlers with autism have altered connectivity in various brain areas and networks, including sensory areas. But most of these data come from ‘baby sibs’ — the younger siblings of autistic children, who are about 20 times more likely to have autism than the general population. “A lot of our early knowledge is from these high-risk samples of infant siblings,” says Benjamin Yerys, assistant professor of psychology in psychiatry at the University of Pennsylvania, who was not involved with the study. “If their behaviors and genetics are different, then all of this early brain work may also be different.” By contrast, the new work focused on autistic children who were newly diagnosed. “There are very, very few studies focused on this age, right around the time the diagnosis can be made,” says Christine Wu Nordahl, associate professor at the University of California, Davis MIND Institute. “I think that is the major strength of the study.” © 2020 Simons Foundation

Keyword: Autism
Link ID: 27345 - Posted: 07.06.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. © 2020 The New York Times Company

Keyword: Movement Disorders; Learning & Memory
Link ID: 27343 - Posted: 07.02.2020

Jason Bruck Human actions have taken a steep toll on whales and dolphins. Some studies estimate that small whale abundance, which includes dolphins, has fallen 87% since 1980 and thousands of whales die from rope entanglement annually. But humans also cause less obvious harm. Researchers have found changes in the stress levels, reproductive health and respiratory health of these animals, but this valuable data is extremely hard to collect. To better understand how people influence the overall health of dolphins, my colleagues and I at Oklahoma State University’s Unmanned Systems Research Institute are developing a drone to collect samples from the spray that comes from their blowholes. Using these samples, we will learn more about these animals’ health, which can aid in their conservation. Today, researchers wanting to measure wild dolphins’ health primarily use remote biopsy darting – where researchers use a small dart to collect a sample of tissue – or handle the animals in order to collect samples. These methods don’t physically harm the animals, but despite precautions, they can be disruptive and stressful for dolphins. Additionally, this process is challenging, time-consuming and expensive. My current research focus is on dolphin perception – how they see, hear and sense the world. Using my experience, I am part of a team building a drone specifically designed to be an improvement over current sampling methods, both for dolphins and the researchers. Our goal is to develop a quiet drone that can fly into a dolphin’s blind spot and collect samples from the mucus that is mixed with water and air sprayed out of a dolphin’s blowhole when they exhale a breath. This is called the blow. Dolphins would experience less stress and teams could collect more samples at less expense. © 2010–2020, The Conversation US, Inc.

Keyword: Learning & Memory; Evolution
Link ID: 27342 - Posted: 07.02.2020

By Veronique Greenwood Planarians have unusual talents, to say the least. If you slice one of the tiny flatworms in half, the halves will grow back, giving you two identical worms. Cut a flatworm’s head in two, and it will grow two heads. Cut an eye off a flatworm — it will grow back. Stick an eye on a flatworm that lacks eyes — it’ll take root. Pieces as small as one-279th of a flatworm will turn into new, whole flatworms, given the time. This process of regeneration has fascinated scientists for more than 200 years, prompting myriad zany, if somewhat macabre, experiments to understand how it is possible for a complex organism to rebuild itself from scratch, over and over and over again. In a paper published Friday in Science, researchers revealed a tantalizing glimpse into how the worms’ nervous systems manage this feat. Specialized cells, the scientists report, point the way for neurons stretching from newly grown eyes to the brain of the worm, helping them connect correctly. The research suggests that cellular guides hidden throughout the planarian body may make it possible for the worm’s newly grown neurons to retrace their steps. Gathering these and other insights from the study of flatworms may someday help scientists interested in helping humans regenerate injured neurons. María Lucila Scimone, a researcher at M.I.T.’s Whitehead Institute for Biomedical Research, first noticed these cells while studying Schmidtea mediterranea, a planarian common to bodies of freshwater in Southern Europe and North Africa. During another experiment, she noted that they were expressing a gene involved in regeneration. The team looked more closely and realized that some of the regeneration-related cells were positioned at key branching points in the network of nerves between the worms’ eyes and their brains. When the researchers transplanted an eye from one animal to another, the neurons growing from the new eye always grew toward these cells. When the nerve cells reached their target, they kept growing along the route that would take them to the brain. Removing those cells meant the neurons got lost and did not reach the brain. © 2020 The New York Times Company

Keyword: Development of the Brain; Regeneration
Link ID: 27340 - Posted: 07.01.2020