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Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.
The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.
Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.
Photo credit: Yoichi Araki, Ph.D.
By Erin Blakemore It’s scientific canard so old it’s practically cliché: When people lose their sight, other senses heighten to compensate. But are there really differences between the senses of blind and sighted people? It’s been hard to prove, until now. As George Dvorsky reports for Gizmodo, new research shows that blind people’s brains are structurally different than those of sighted people. In a new study published in the journal PLOS One, researchers reveal that the brains of people who are born blind or went blind in early childhood are wired differently than people born with their sight. The study is the first to look at both structural and functional differences between blind and sighted people. Researchers used MRI scanners to peer at the brains of 12 people born with “early profound blindness”—that is, people who were either born without sight or lost it by age three, reports Dvorsky. Then they compared the MRI images to images of the brains of 16 people who were born with sight and who had normal vision (either alone or with corrective help from glasses). The comparisons showed marked differences between the brains of those born with sight and those born without. Essentially, the brains of blind people appeared to be wired differently when it came to things like structure and connectivity. The researchers noticed enhanced connections between some areas of the brain, too—particularly the occipital and frontal cortex areas, which control working memory. There was decreased connectivity between some areas of the brain, as well.
By Scott Barry Kaufman Rarely do I read a scientific paper that overwhelms me with so much excitement, awe, and reverence. Well, a new paper in Psychological Science has really got me revved up, and I am bursting to share their findings with you! Most research on mind-wandering and daydreaming draws on either two methods: strict, laboratory conditions that ask people to complete boring, cognitive tasks and retrospective surveys that ask people to recall how often they daydream in daily life. It has been rather difficult to compare these results to each other; laboratory tasks aren't representative of how we normally go about our day, and surveys are prone to memory distortion. In this new, exciting study, Michael Kane and colleagues directly compared laboratory mind-wandering with real-life mind wandering within the same person, and used an important methodology called "experience-sampling" that allows the researcher to capture people's ongoing stream of consciousness. For 7 days, 8 times a day, the researchers randomly asked 274 undergraduates at North Carolina at Greensboro whether they were mind-wandering and the quality of their daydreams. They also asked them to engage in a range of tasks in the laboratory that assessed their rates of mind-wandering, the contents of their off-task thoughts, and their "executive functioning" (a set of skills that helps keep things in memory despite distractions and focus on the relevant details). What did they find? © 2017 Scientific American
Link ID: 23409 - Posted: 03.27.2017
By Melissa Banigan Twenty years ago, I started experiencing what turned into a long list of seemingly unrelated health issues. Headaches, depression, insomnia, peripheral neuropathy, fatigue, joint pain, chest pain, shortness of breath, a lesion on my spine and a variety of uncomfortable gastrointestinal ailments. Over the past five years, things went from bad to worse as I also became lactose-intolerant, developed mild vitiligo (a condition that leads to loss of skin pigmentation) and major vertigo, experienced a series of low-grade fevers and started to have some memory loss that I referred to as brain fogs. Doctors told me that as an overworked single mother of 40, I might just need to figure out ways to get more sleep and relax. Some of what was happening, they said, might be attributed to the normal processes of aging. What was happening, however, didn’t feel normal. Always a voracious reader and a writer by profession, I could no longer focus on work, read even a page of a book or grip a pen long enough to write a grocery list. I often felt too exhausted to keep plans with friends. When I did pull myself off my couch to see them, I couldn’t concentrate on conversations, so I sequestered myself in my apartment and let my friendships fade. I had been a runner, a swimmer and a hiker, but just walking up a flight of stairs made me lose my breath so completely that I succumbed to inactivity. I did everything the doctors asked me to do. I changed my diet and sleep schedule, went to a physical therapist and saw specialists in neurology and rheumatology and even a mental-health therapist. I then also turned to massage therapists, herbalists and an acupuncturist. © 1996-2017 The Washington Post
Austin Frakt By middle age, the lenses in your eyes harden, becoming less flexible. Your eye muscles increasingly struggle to bend them to focus on this print. But a new form of training — brain retraining, really — may delay the inevitable age-related loss of close-range visual focus so that you won’t need reading glasses. Various studies say it works, though no treatment of any kind works for everybody. The increasing difficulty of reading small print that begins in middle age is called presbyopia, from the Greek words for “old man” and “eye.” It’s exceedingly common, and despite the Greek etymology, women experience it, too. Every five years, the average adult over 30 loses the ability to see another line on the eye reading charts used in eye doctors’ offices. By 45, presbyopia affects an estimated 83 percent of adults in North America. Over age 50, it’s nearly universal. It’s why my middle-aged friends are getting fitted for bifocals or graduated lenses. There are holdouts, of course, who view their cellphones and newspapers at arm’s length to make out the words. The decline in vision is inconvenient, but it’s also dangerous, causing falls and auto accidents. Bifocals or graduated lenses can help those with presbyopia read, but they also contribute to falls and accidents because they can impair contrast sensitivity (the ability to distinguish between shades of gray) and depth perception. I’m 45. I don’t need to correct my vision for presbyopia yet, but I can tell it’s coming. I can still read the The New York Times print edition with ease, but to read text in somewhat smaller fonts, I have to strain. Any year now, I figured my eye doctor would tell me it was time to talk about bifocals. Or so I thought. Then I undertook a monthslong, strenuous regimen designed to train my brain to correct for what my eye muscles no longer can manage. © 2017 The New York Times Company
Link ID: 23407 - Posted: 03.27.2017
By STEPH YIN For animals that hibernate, making it to spring is no small feat. Torpor — the state of reduced bodily activity that occurs during hibernation — is not restful. By the time they emerge, hibernating animals are often sleep-deprived: Most expend huge bursts of energy to arouse themselves occasionally in the winter so their body temperatures don’t dip too low. This back-and-forth is exhausting, and hibernators do it with little to no food and water. By winter’s end, some have shed more than half their body weight. But just because it’s spring doesn’t mean it’s time to celebrate. Spring means getting ready for the full speed of summer — and after spending a season in slow motion, that requires some ramping up. Here’s a look at what different animals have on the agenda after coming out of winter’s slumber. Black bears emerge from their dens in April, but stay lethargic for weeks. During this so-called walking hibernation, they sleep plenty and don’t roam very far. Though they have lost up to one-third of their body weight over winter, they don’t have a huge appetite right away — their metabolism is not yet back to normal. They snack mostly on pussy willows and bunches of snow fleas. In January or February, some females give birth, typically to two or three cubs. New mothers continue to hibernate, but they go in and out of torpor, staying alert enough to respond to their cubs’ cries. When they emerge from their dens, mama bears find trees with rough bark that her cubs can easily climb for safety. “Slowly, the bears’ metabolism gears up to normal, active levels,” said Lynn Rogers, a bear expert and principal biologist at the Wildlife Research Institute, a nonprofit in Minnesota. “When plants start sprouting on the forest floor, that’s when they start really moving around.” © 2017 The New York Times Company
Keyword: Biological Rhythms
Link ID: 23406 - Posted: 03.25.2017
By Diana Kwon Astrocytes, star-shape glial cells in the brain, were once simply considered support cells for neurons. However, neuroscientists have recently realized they have many other functions: studies have shown that astrocytes are involved in metabolism, learning, and more. In the latest study to investigate astrocytes’ roles in the brain, researchers confirmed these cells played a key role in regulating mouse circadian rhythms. The team’s results were published today (March 23) in Current Biology. “Recent results have indicated that [glia] are actively modulating synaptic transmission, the development of the nervous system, and changes in the nervous system in response to changes in the environment,” said coauthor Erik Herzog, a neuroscientist at Washington University in St. Louis. “So circadian biologists recognized that the system that we study in the brain also had astrocytes and have wondered what role that they might play.” In 2005, Herzog’s team published a seminal study linking glia to mammalian circadian rhythms. By investigating rat and mouse astrocytes in a dish, the researchers discovered that these glial cells showed circadian rhythms in gene expression. Since then, several independent groups have reported evidence to suggest that astrocytes help regulate daily rhythms. However, linking astrocytes to circadian behaviors in mice remained difficult. “I had several folks in the lab over many years [who] were unable to find the tools that would allow us to answer the question definitively: Do astrocytes play a role in scheduling our day?” Herzog recalled. “Then, within the last year or so, some new tools . . . became available for us.”. © 1986-2017 The Scientist
USA Today Network Josh Hafner , For college students, new parents and employees dogged by deadlines, the all-nighter is nothing new. But going without sleep leaves you basically drunk, putting you at the equivalent of a .1% blood alcohol content as you drive to work, make decisions and interact with others. “The first thing that goes is your ability to think," said Joseph Ojile, M.D., a board member with the National Sleep Foundation. Judgement, memory and concentration all suffer impairment by the body's 17th hour without sleep, he said. “We know at 17 hours, you're at .08% blood alcohol level," he said, the legal standard for drunk driving. "At 24 hours, you’re at 0.1%." Coordination deteriorates as well in those intervening hours, said Ojile, a professor at Saint Louis University School of Medicine. Irritability sets in, too. Pain becomes more acute and the immune system suffers, he said, leaving the body more open to infection. "Here’s the worst part about the lack of judgement," Ojile said. "The person is unaware of their impairment. How scary is that? ‘I’m fine, I’ll just drive home. I’ll do my work at the nuclear plant, no problem. Or fly the plane, no problem.’" It's not entirely clear how the effects worsen past 24 hours, Ojile said, other than they do. The brain starts shutting down in trance-like microsleeps, 15- to 30-second spells that occur without the person noticing. Eventually, not sleeping results in death.
Link ID: 23404 - Posted: 03.25.2017
By Linda Searing The precise cause, or causes, of dementias such as Alzheimer’s disease remain unclear, but one theory points to molecules called free radicals that can damage nerve cells. This damage, called oxidative stress, may lead to changes in the brain over time that result in dementia. Might antioxidant supplements prevent this? The study involved 7,540 men 60 and older (average age, 67) with no indications of dementia and no history of serious head injury, substance abuse or neurological conditions that affect cognition. They were randomly assigned to take vitamin E (an antioxidant, 400 International Units daily), selenium (also an antioxidant, 200 micrograms daily), both vitamin E and selenium or a placebo. The men also had their memory assessed periodically. In just over five years, 325 of the men (about 4 percent) developed dementia, with essentially no difference in the rate of occurrence between those who took one or both supplements and those who took the placebo. The researchers concluded that the antioxidant supplements “did not forestall dementia and are not recommended as preventive agents.” Who may be affected? Older men. The risk for dementia increases with advanced age and is most common among the very elderly. Memory loss is the most well-known symptom, but people with dementia may also have problems thinking, speaking, controlling emotions and doing daily activities such as getting dressed and eating. Alzheimer’s disease is the most common type of dementia, affecting more than 5.5 million Americans, including more than 10 percent of those 65 and older and more women than men. Caveats Participants took the supplements for a relatively short time. Whether the findings would apply to women was not tested. The study did not prove that the dementia developed by the study participants was caused by oxidative stress. © 1996-2017 The Washington Post
Link ID: 23403 - Posted: 03.25.2017
By Anil Ananthaswamy People who have chronic pain are more likely to experience mood disorders, but it’s not clear how this happens. Now a study in mice has found that chronic pain can induce genetic changes in brain regions that are linked to depression and anxiety, a finding that may lead to new treatments for pain. “At least 40 per cent of patients who suffer from severe forms of chronic pain also develop depression at some point, along with other cognitive problems,” says Venetia Zachariou of the Icahn School of Medicine at Mount Sinai in New York. To see if there might be a genetic link between these conditions, Zachariou and her team studied mice with damage to their peripheral nervous system. These mice show symptoms similar to chronic pain in people – they become hypersensitive to harmless touch, and avoid other situations that might also cause them pain. Until now, pain behaviour in mice had only been studied for at most a week at a time, says Zachariou, whose team monitored their mice for 10 weeks. “At the beginning, we saw only sensory deficits and pain-like symptoms. But several weeks later, the animals developed anxiety and depression-like behaviours.” The team then examined gene activity in three regions in the mouse brains we know are associated with depression and anxiety. Analysing the nucleus accumbens, medial prefrontal cortex, and periaqueductal gray, they found nearly 40 genes where activity was significantly higher or lower than in mice without the nervous system damage. © Copyright Reed Business Information Ltd.
By Jason G. Goldman In the summer of 2015 University of Oxford zoologists Antone Martinho III and Alex Kacelnik began quite the cute experiment—one involving ducklings and blindfolds. They wanted to see how the baby birds imprinted on their mothers depending on which eye was available. Why? Because birds lack a part of the brain humans take for granted. Suspended between the left and right hemispheres of our brains sits the corpus callosum, a thick bundle of nerves. It acts as an information bridge, allowing the left and right sides to rapidly communicate and act as a coherent whole. Although the hemispheres of a bird's brain are not entirely separated, the animals do not enjoy the benefits of this pathway. This quirk of avian neuroanatomy sets up a natural experiment. “I was in St. James's Park in London, and I saw some ducklings with their parents in the lake,” Martinho says. “It occurred to me that we could look at the instantaneous transfer of information through imprinting.” The researchers covered one eye of each of 64 ducklings and then presented a fake red or blue adult duck. This colored duck became “Mom,” and the ducklings followed it around. But when some of the ducklings' blindfolds were swapped so they could see out of only the other eye, they did not seem to recognize their “parent” anymore. Instead the ducklings in this situation showed equal affinity for both the red and blue ducks. It took three hours before any preferences began to emerge. Meanwhile ducklings with eyes that were each imprinted to a different duck did not show any parental preferences when allowed to use both eyes at once. The study was recently published in the journal Animal Behaviour. © 2017 Scientific American
If your parrot is feeling glum, it might be tweetable. Wild keas spontaneously burst into playful behaviour when exposed to the parrot equivalent of canned laughter – the first birds known to respond to laughter-like sounds. The parrots soared after one another in aerobatic loops, exchanged foot-kicking high fives in mid-air and tossed objects to each other, in what seems to be emotionally contagious behaviour. And when the recording stops, so does the party, and the birds go back to whatever they had been doing. We already knew that these half-metre-tall parrots engage in playful behaviour, especially when young. What’s new is that a special warbling call they make has been shown to trigger behaviour that seems to be an equivalent of spontaneous, contagious laughter in humans. Moreover, it’s not just the young ones that respond, adults of both sexes join in the fun too. Raoul Schwing of the University of Veterinary Medicine in Vienna, Austria, and his team played 5-minute recordings to gatherings of between two and a dozen wild keas on a mountainside of New Zealand’s Arthur’s Pass National Park, on the southern island. The group played recordings of the warble sound, or other sounds, including two other frequent kea sounds – a screech and a whistle – plus the alarm call of a local robin species and a bland tone. © Copyright Reed Business Information Lt
By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company
by Laura Sanders Many babies born early spend extra time in the hospital, receiving the care of dedicated teams of doctors and nurses. For these babies, the hospital is their first home. And early experiences there, from lights to sounds to touches, may influence how babies develop. Touches early in life in the NICU, both pleasant and not, may shape how a baby’s brain responds to gentle touches later, a new study suggests. The results, published online March 16 in Current Biology, draw attention to the importance of touch, both in type and number. Young babies can’t see that well. But the sense of touch develops early, making it a prime way to get messages to fuzzy-eyed, pre-verbal babies. “We focused on touch because it really is some of the basis for communication between parents and child,” says study coauthor Nathalie Maitre, a neonatologist and neuroscientist at Nationwide Children’s Hospital in Columbus, Ohio. Maitre and her colleagues studied how babies’ brains responded to a light puff of air on the palms of their hands — a “very gentle and very weak touch,” she says. They measured these responses by putting adorable, tiny electroencephalogram, or EEG, caps on the babies. The researchers puffed babies’ hands shortly before they were sent home. Sixty-one of the babies were born early, from 24 to 36 weeks gestation. At the time of the puff experiment, they had already spent a median of 28 days in the hospital. Another group of 55 babies, born full-term, was tested in the three days after birth. |© Society for Science & the Public 2000 - 2017
/ By Katie Rose Quandt One afternoon in 2013, after swimming and playing outside, 9-year-old Taylor Johnson, from outside Atlanta, began sneezing incessantly. The fit lasted days before stopping abruptly, only to return months later. For a year, her violent sneezing fits came and went, to the bewilderment of a series of doctors. For families, the diagnosis can seem like an answer to their prayers. But there’s a catch: Most doctors won’t treat the diseases — and many don’t believe they even exist. “She was making this noise with her mouth at times 140 to 150 times a minute,” said her mother, Lori Johnson. “She was frantic, she couldn’t eat, she couldn’t sleep.” And “when she wasn’t sneezing, she was very depressed… She lost all interest in anything. Her whole personality just dissolved into nothing.” Then an otolaryngologist (an ear, nose, and throat doctor) realized Taylor wasn’t sneezing at all — the behavior was a repetitive, sneeze-like tic. That prompted a round of visits to neurologists, psychologists, and other specialists, until an allergist finally suggested a set of diagnoses unfamiliar to the Johnsons: PANS and PANDAS. These disorders, a specialist told them, can arise in certain predisposed children when the immune system responds to an infection like strep throat by attacking the brain. The resulting inflammation can lead to violent body tics and OCD-like symptoms. Copyright 2017 Undark
A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017
By Jia Naqvi A drug frequently prescribed for pain is no more effective than a placebo at controlling sciatica, a common source of pain in the lower back and leg, according to a study published Wednesday in the New England Journal of Medicine. The researchers at the George Institute for Global Health in Australia followed 209 sciatica patients in Sydney who were randomly assigned to receive either the drug pregabalin, more commonly known as Lyrica, or a placebo. The results showed no significant differences in leg pain intensity between the group on the placebo and that on Lyrica after eight weeks taking the drug or during the rest of the year on follow-up exams. Similarly, there were no differences for other outcomes such as back pain, quality of life and degree of disability. After Lyrica was approved in 2004, it has become the most commonly prescribed medicine for neuropathic pain, which is caused by damage to the nervous system. The drug was ranked as the 19th-highest-earning pharmaceutical in 2015, with worldwide sales rising annually at a rate of 9 percent and sale revenue of more than $3 billion in 2015 in the United States. “We have seen a huge rise in the amount of prescriptions being written each year for patients suffering from sciatica. It’s an incredibly painful and disabling condition, so it’s no wonder people are desperate for relief and medicines such as pregabalin have been widely prescribed,” Christine Lin, one of the authors of the study and an associate professor at the George Institute for Global Health, said in a news release. © 1996-2017 The Washington Post
Keyword: Pain & Touch
Link ID: 23395 - Posted: 03.23.2017
By Sam Wong It takes brains to choose a good partner. In one of the first experiments to look at the cognitive demands of choosing a mate, female guppies with big brains showed a preference for more colourful males, while those with smaller brains showed no preference. In guppies, like most animals, females are choosy about who to mate with, since they invest more in their offspring than males, which don’t help care for them. They tend to prefer males with striking colour patterns and big tails, traits that have been linked to good foraging ability and health. By choosing a male with these qualities, female guppies give their offspring a good chance of inheriting the same useful traits. Despite this, females often go on to make different choices. Alberto Corral López and colleagues at Stockholm University wanted to find out if brain size could account for this. Corral López and his team tested 36 females bred to have large brains, 36 bred to have small brains, and 16 females similar to guppies found in the wild. Previous studies have shown that large-brained guppies perform better in cognitive tests, suggesting that they are smarter. Each female was given the opportunity to associate with two males, one more colourful than the other. Females are known to spend more time close to males they would prefer to mate with, so the team timed how long they spent with each male. © Copyright Reed Business Information Ltd
By Daisy Yuhas, Spectrum on March 22, 2017 In children with a deletion on chromosome 22, having autism does not boost the risk of developing schizophrenia later in life, according to a new study1. The children in the study have 22q11.2 deletion syndrome, which is linked to a 25-fold increase in the risk of developing a psychotic condition such as schizophrenia. A deletion in the region is also associated with an increased risk of autism. Some researchers have suggested that the relatively high autism prevalence in this population is the result of misdiagnoses of early signs of schizophrenia. The new findings, published 21 January in Schizophrenia Research, support an alternate theory: Autism and schizophrenia are independent outcomes of the same genetic syndrome. If there is a relationship between the two conditions, “that can only be a very small, probably negligible effect,” says lead investigator Jacob Vorstman, assistant professor of child psychiatry and genetics at the University Medical Center Utrecht in the Netherlands. The new findings could help guide clinical care, says Opal Ousley, assistant professor of psychiatry at the Emory Autism Center in Atlanta. If prenatal testing picks up the 22q11.2 deletion, for instance, clinicians could discuss the risk of both autism and schizophrenia with parents. © 2017 Scientific American
By David Wiegand I just did something great for my brain and you can do the same, when the documentary “My Love Affair With the Brain: The Life and Science of Dr. Marian Diamond” airs on KQED on Wednesday, March 22. According to the UC Berkeley professor emerita, the five things that contribute to the continued development of the brain at any age are: diet, exercise, newness, challenge and love. You can check off three of those elements for the day by watching the film by Catherine Ryan and Gary Weimberg. No matter how smart you are, even about anatomy and neuroscience, you will find newness in the information about the miraculous human brain, how it works, and how it keeps on working no matter how old you are. That’s one of the fundamentals of modern neuroscience, of which Diamond is one of the founders. You will also be challenged to consider your own brain, to consider how Diamond’s favorite expression — “use it or lose it” — applies to your brain and your life. You will be challenged to consider what Diamond means when she says brain plasticity (its ability to keep developing by forming new connections between its cells) makes us “the masters of our own minds. We literally create our own masterpiece.” Before Diamond and her colleagues proved otherwise, the prevailing thought was that brains developed according to a genetically determined pattern, hit a high point and then essentially began to deteriorate. Bushwa: A brain can grow — i.e., learn — at any age, and you can teach an old dog new tricks. © 2017 Hearst Corporation
Keyword: Learning & Memory
Link ID: 23392 - Posted: 03.23.2017
By Mo Costandi This map of London shows how many other streets are connected to each street, with blue representing simple streets with few connecting streets and red representing complex streets with many connecting streets. Credit: Joao Pinelo Silva The brain contains a built-in GPS that relies on memories of past navigation experiences to simulate future ones. But how does it represent new environments in order to determine how to navigate them successfully? And what happens in the brain when we enter a new space, or use satellite navigation (SatNav) technology to help us find our way around? Research published Tuesday in Nature Communications reveals two distinct brain regions that cooperate to simulate the topology of one’s environment and plan future paths through it when one is actively navigating. In addition, the research suggests both regions become inactive when people follow SatNav instructions instead of using their spatial memories. In a previous study researchers at University College London took participants on a guided tour through the streets of London’s Soho district and then used functional magnetic resonance imaging (fMRI) to scan their brains as they watched 10 different simulations of navigating those streets. Some of the movies required them to decide at intersections which way would be the shortest path to a predetermined destination; others came with instructions about which way to go at each junction. © 2017 Scientific American,
Keyword: Learning & Memory
Link ID: 23391 - Posted: 03.22.2017