Chapter 13. Memory, Learning, and Development

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Tina Hesman Saey A genetic risk factor for Alzheimer’s disease is a double, make that triple, whammy. In addition to speeding up the development of brain plaques associated with Alzheimer’s, a gene variant known as APOE4 also makes tau tangles — another signature of the disease — worse, researchers report online September 20 in Nature. APOE4 protein also ramps up brain inflammation that kills brain cells, neuroscientist David Holtzman of Washington University School of Medicine in St. Louis and colleagues have discovered. “This paper is a tour de force,” says Robert Vassar, a neuroscientist at Northwestern University Feinberg School of Medicine in Chicago. “It’s a seminal study that’s going to be a landmark in the field” of Alzheimer’s research, Vassar predicts. For more than 20 years, researchers have known that people who carry the E4 version of the APOE gene are at increased risk of developing Alzheimer’s. A version of the gene called APOE3 has no effect on Alzheimer’s risk, whereas the APOE2 version protects against the disease. Molecular details for how APOE protein, which helps clear cholesterol from the body, affects brain cells are not understood. But Holtzman and other researchers previously demonstrated that plaques of amyloid-beta protein build up faster in the brains of APOE4 carriers (SN: 7/30/11, p. 9). Having A-beta plaques isn’t enough to cause the disease, Holtzman says. Tangles of another protein called tau are also required. Once tau tangles accumulate, brain cells begin to die and people develop dementia. In a series of new experiments, Holtzman and colleagues now show, for the first time, that there’s also a link between APOE4 and tau tangles. |© Society for Science & the Public 2000 - 2017.

Keyword: Alzheimers
Link ID: 24103 - Posted: 09.23.2017

By Ruth Williams Contrary to the longstanding belief that puberty is largely controlled by hormones, new evidence shows that sexual touch is a powerful puberty promoter. Touching prepubescent female rats’ genitals can cause the brain region that responds to such tactile stimuli to double in size and their bodies to show signs of puberty up to three weeks earlier than non-stimulated females, according to a report in PLOS Biology today (September 21). The study reveals the hitherto unappreciated influence of physical sexual experience on the young brain and body. “The dominant idea has been that puberty is controlled in the brain and in behavior by the release of hormones . . . but there has been a smattering of findings over the years that additional environmental influences effect puberty and the onset of sexual behavior,” says Dan Feldman of the University of California, Berkeley, who was not involved in the study. This new work “suggests that maybe this is true and that actual tactile stimulation can be something that accelerates the onset of puberty,” he adds. Puberty in mammals is a period of dramatic changes not just to the body, but to behavior and brain function. Indeed, one of the most pronounced changes, recently observed in both male and female rats, is the doubling in size of the genital cortex, which is a part of the larger somatosensory cortex—the brain area associated with physical sensation. © 1986-2017 The Scientist

Keyword: Sexual Behavior; Development of the Brain
Link ID: 24102 - Posted: 09.23.2017

By Ann Gibbons Neandertals have long been seen as the James Deans of human evolution—they grew up fast, died young, and became legends. But now, a rare skeleton of a Neandertal child suggests that our closest cousins didn’t all lead such fast lives—and that our own long childhoods aren’t unique. The find may reveal how Neandertals, like humans, had enough energy to grow bigger brains. “We like the paper because it puts the idea of ‘Neanderthal exceptionalism’ to rest,” wrote anthropologist Marcia Ponce de León and neurobiologist Christoph Zollikofer from the University of Zurich in Switzerland (who are not authors of the new study) in an email. “RIP.” Researchers have long known that modern humans take almost twice as long as chimpanzees to reach adulthood and have wondered when and why our ancestors evolved the ability to prolong childhood and delay reproduction. Our distant ancestors, such as the famous fossil Lucy and other australopithecines, matured quickly and died young like chimps. Even early members of our own genus Homo, such as the 1.6-million-year-old skeleton of an H. erectus boy, grew up faster than we do. By providing your email address, you agree to send your email address to the publication. Information provided here is subject to Science's Privacy Policy. But by the time the earliest known members of our species, H. sapiens, were alive 300,000 years ago at Jebel Irhoud in Morocco, they were taking longer to grow up. A leading theory is that big brains are so metabolically expensive that humans have to delay the age of reproduction—and, hence, have longer childhoods—so first-time mothers are older and, thus, bigger and strong enough to have the energy to feed babies with such big brains after birth when their brains are doubling in size. © 2017 American Association for the Advancement of Science

Keyword: Evolution; Development of the Brain
Link ID: 24098 - Posted: 09.22.2017

By Gary Stix Donald Hebb was a famed Canadian scientist who produced key findings that ranged across the field of psychology, providing insights into perception, intelligence and emotion. He is perhaps best known, though, for his theory of learning and memory, which appears as an entry in most basic texts on neuroscience. But now an alternative theory—along with accompanying experimental evidence—fundamentally challenges some central tenets of Hebb’s thinking. It provides a detailed account of how cells and the electrical and molecular signals that activate them are involved in forming memories of a series of related events. Put forward in 1949, Hebb’s theory holds that when electrical activity in one neuron—perhaps triggered by observing one’s surroundings—repeatedly induces a neighboring “target cell” to fire electrical impulses, a process of conditioning occurs and strengthens the connection between the two neurons. This is a bit like doing arm curls with a weight; after repeated lifts the arm muscle grows stronger and the barbell gets easier to hoist. At the cellular level, repeated stimulation of one neuron by another enables the target cell to respond more readily the next time it is activated. In basic textbooks, this boils down to a simple adage to describe the physiology of learning and memory: “Cells that fire together, wire together.” Every theory requires experimental evidence, and scientists have toiled for years to validate Hebb’s idea in the laboratory. Many research findings have showed that when a neuron repeatedly fires off an electrical impulse (called an “action potential”) at virtually the same time as an adjacent neuron, their connection does indeed grow more efficient. The target cell fires more easily, and the signal transmitted is stronger. This process—known as long-term potentiation (LTP)—apparently induces physiological change or “plasticity” in target cells. LTP is routinely cited as a possible explanation for how the brain learns and forms memories at the cellular level. © 2017 Scientific American,

Keyword: Learning & Memory
Link ID: 24093 - Posted: 09.21.2017

By Alla Katsnelson, Men and women both transmit an increasing number of new mutations to their children as they age, according to a study published today in Nature1. The finding is based on an analysis of whole genomes from nearly 5,000 people. The increase in these ‘de novo’ mutations may explain why older parents are more likely to have a child with a condition such as autism. Men accumulate de novo mutations four times faster than women, the researchers found. However, in about 10 percent of the genome, mutations accumulate twice as quickly as elsewhere, and appear at an equal rate in both women and men. “The majority of the contribution still comes from the father, particularly when the father is in an older age range,” says lead investigator Kári Stefánsson, chief executive of deCODE Genetics. “But the mutation rate is not equal across the genome, so we have to make sure we do not generalize too much.” The new study builds on earlier work by deCODE Genetics, a company based in Reykjavik, Iceland. In 2012, the researchers reported that the rate at which people acquire mutations and pass them down to their children increases sharply with age in men but stays level in women. Those findings were based on whole-genome sequences from just 78 individuals and their parents. The findings provide one possible explanation for the increased risk of autism among children born to older parents. © 2017 Scientific American

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 24091 - Posted: 09.21.2017

by Emilie Reas Paranoia. Munchies. Giggles. Sleepiness. Memory loss. Although the effects of cannabinoids–the active components of marijuana–are familiar to many, their neurobiological substrates are poorly characterized. Perhaps the effect of greatest interest to both neuroscientists and to cannabis users hoping to preserve their cognitive function, is short-term memory impairment that often accompanies marijuana use. Our partial understanding of its physiological and behavioral effects is not for want of studies into its neural effects. Ample research has shown a range of changes to neurotransmission, receptors, ion channels and mitochondria following cannabinoid exposure. However, knowledge of its cellular and molecular properties alone cannot offer a complete picture of its system-wide effects leading to cognitive and behavioral changes. A recent study published in PLOS Computational Biology took a novel approach to address this issue, combining computational modeling with electrophysiological brain recordings from rats performing a memory task, to unravel the dynamics of neural circuits under the influence of cannabinoids. To assess memory changes induced by cannabinoids, the scientists injected tetrahydrocannabinol (THC), the main psychoactive compound in marijuana, into rats before they performed a “delayed-nonmatch-to-sample” working memory task. In this task, rats are cued with one of two levers, and after a delay, are required to select the opposite lever. Compared to sober sessions, performance under THC was impaired by 12%, confirming the all-too-familiar memory impairment associated with cannabis use. THC alters hippocampal activity

Keyword: Learning & Memory; Drug Abuse
Link ID: 24087 - Posted: 09.21.2017

By Deborah Tuerkheimer Controversy surrounding “shaken baby syndrome” (SBS) is taking centre stage again. The American Academy of Pediatrics (AAP) meets today with a session underscoring the message that most paediatricians – child abuse specialists among them – say it remains a “valid” diagnosis. In other words, the paediatric community continues to believe that shaking can bring about one or more of the classic triad of neurological symptoms: bleeding beneath the outer layer of membranes surrounding the brain, bleeding in the retina, and brain swelling. This is likely to prompt vigorous opposition from those within the medical community who challenge the scientific underpinnings of SBS. It is also likely to resonate with the public, many of whom assume that this diagnosis alone amounts to proof beyond a reasonable doubt that a caregiver or parent injured or killed a baby by violent shaking. It does not. Yet for decades such prosecutions did rest on the testimony of medical experts regarding the triad. Doctors came to court and explained that vigorous shaking – not an accidental jostle or an effort to revive an unconscious child – was the only possible explanation for those symptoms. The triad was even used to identify a perpetrator – whoever was last with the lucid baby. SBS could, in essence, be a medical diagnosis of murder. Beginning in the 1990s, triad-only prosecutions became increasingly commonplace, sending many caregivers to prison. © Copyright New Scientist Ltd.=

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 24082 - Posted: 09.20.2017

Daniel Cressey Many sharks are living much longer than was thought, according to a major review1 of studies on these important and often endangered top predators. This means that many estimates of how threatened particular species are — and decisions about whether they can be fished safely — could be based on faulty data. Scientists usually estimate how old sharks are by slicing through their spines and counting distinctive pairs of bands seen inside, which are often assumed to show age in the same way as the rings of a tree. But a growing number of cases are suggesting that the method can be problematic. For example, a 2014 study2 showed that sand tiger sharks (Carcharias taurus), which were thought to live for around two decades, can actually survive for up to twice that. And in 2007, researchers found3 that New Zealand porbeagle sharks (Lamna nasus) had been under-aged by an average of 22 years. To investigate the scale of the problem, fisheries researcher Alastair Harry of James Cook University in Townsville, Australia, reviewed evidence for age underestimation. He reports in Fish and Fisheries1 that of 53 populations of sharks and rays for which there are good data, 30% have probably had their ages underestimated (see graphic). “Current evidence points to it being systemic, rather than restricted to a few isolated cases,” says Harry. “We really can’t ignore it anymore.” © 2017 Macmillan Publishers Limited,

Keyword: Development of the Brain
Link ID: 24081 - Posted: 09.20.2017

By Marissa Fessenden, A new technique classifies neurons by surveying chemical tags that turn genes on or off on the neurons’ DNA1. The approach represents a new way to chart the brain’s cellular diversity. It could reveal how patterns of chemical tags known as methyl groups are altered in autism. Methyl groups bind to the DNA base cytosine. Patterns of methylation can be inherited, but they can also change in response to environmental factors, such as exposure in the womb to stress hormones or to the mother’s diet. Studies have reported altered methylation patterns in postmortem brains of people with autism. Methylation patterns also vary by cell type. In a new study, published 11 August in Science, researchers classified neurons from mouse and human brain tissue by their methylation patterns. The researchers looked at cells from specific layers of the brain’s outer shell, the cerebral cortex. They used a chemical cocktail to isolate the cells’ nuclei, and placed a single nucleus in each well of a 384-well plate. They then treated the nuclei with a chemical that converts cytosines without methyl groups to the RNA base uracil. They sequenced the DNA to pinpoint the remaining cytosines, yielding a map of every methyl group. © 2017 Scientific American,

Keyword: Epigenetics; Development of the Brain
Link ID: 24073 - Posted: 09.19.2017

Allison Aubrey Earlier this year, when Emily Chodos was about 25 weeks into her pregnancy, she woke up one night feeling horrible. "My hands were tremoring, my heart racing, " recalls Chodos, who lives near New Haven, Conn. She couldn't take a deep breath. "I'd never felt so out of control of my body." She ended up paging her obstetrician's office at 4 a.m., and one of the midwives in the practice, after listening to her symptoms, said, "It sounds like you're having a panic attack." Chodos was advised to take an antianxiety medication — Xanax. "I was afraid to take it, as a pregnant woman," Chodos says. But she was miserable, so eventually decided to take the medicine that night. Chodos, who is a nurse, knew that there are concerns about drugs like Xanax and other medications its class— benzodiazepines. Studies completed decades ago suggested a risk of birth defects from these drugs, but data from more recent studies have shown no clear evidence of an increase. There are remaining questions, researchers say, about whether prenatal exposure to the drugs can influence behavior. "I felt very trapped," Chodos says. It felt as if there was probably no safe medication — "that I'd probably just have to suffer and feel awful." At her doctor's suggestion, Chodos went to see Dr. Kimberly Yonkers, a psychiatrist and professor at Yale University. Yonkers has been studying the effects of benzodiazepines and SSRI antidepressants on the pregnancies of women who have anxiety, depression or panic disorders. Yonkers told us she understands why women can feel torn about using these drugs when they're expecting.

Keyword: Depression; Development of the Brain
Link ID: 24070 - Posted: 09.18.2017

By Anil Ananthaswamy Artificial intelligence can identify changes in the brains of people likely to get Alzheimer’s disease almost a decade before doctors can diagnose the disease from symptoms alone. The technique uses non-invasive MRI scans to identify alterations in how regions of the brain are connected. Alzheimer’s is a neurodegenerative disease that is the leading cause of dementia for the elderly, eventually leading to loss of memory and cognitive functions. The race is on to diagnose the disease as early as possible. Although there is no cure, drugs in development are likely to work better the earlier they are given. An early diagnosis can also allow people to start making lifestyle changes to help slow the progression of the disease. When will we cure Alzheimer’s? Learn more at New Scientist Live In an effort to enable earlier diagnosis, Nicola Amoroso and Marianna La Rocca at the University of Bari in Italy and their colleagues developed a machine-learning algorithm to discern structural changes in the brain caused by Alzheimer’s disease. First, they trained the algorithm using 67 MRI scans, 38 of which were from people who had Alzheimer’s and 29 from healthy controls. The scans came from the Alzheimer’s Disease Neuroimaging Initiative database at the University of Southern California in Los Angeles. © Copyright New Scientist Ltd.

Keyword: Alzheimers
Link ID: 24067 - Posted: 09.15.2017

Aaron E. Carroll Many high-school-aged children across the United States now find themselves waking up much earlier than they’d prefer as they return to school. They set their alarms, and their parents force them out of bed in the morning, convinced that this is a necessary part of youth and good preparation for the rest of their lives. It’s not. It’s arbitrary, forced on them against their nature, and a poor economic decision as well. The National Heart, Lung and Blood Institute recommends that teenagers get between nine and 10 hours of sleep. Most in the United States don’t. It’s not their fault. My oldest child, Jacob, is in 10th grade. He plays on the junior varsity tennis team, but his life isn’t consumed by too many extracurricular activities. He’s a hard worker, and he spends a fair amount of time each evening doing homework. I think most nights he’s probably asleep by 10 or 10:30. His school bus picks him up at 6:40 a.m. To catch it, he needs to wake up not long after 6. Nine hours of sleep is a pipe dream, let alone 10. There’s an argument to be made that we should cut back on his activities or make him go to bed earlier so that he gets more sleep. Teens aren’t wired for that, though. They want to go to bed later and sleep later. It’s not the activities that prevent them from getting enough sleep — it’s the school start times that require them to wake up so early. More than 90 percent of high schools and more than 80 percent of middle schools start before 8:30 a.m. Some argue that delaying school start times would just cause teenagers to stay up later. Research doesn’t support that idea. A systematic review published a year ago examined how school start delays affect students’ sleep and other outcomes. Six studies, two of which were randomized controlled trials, showed that delaying the start of school from 25 to 60 minutes corresponded with increased sleep time of 25 to 77 minutes per week night. In other words, when students were allowed to sleep later in the morning, they still went to bed at the same time, and got more sleep. © 2017 The New York Times Company

Keyword: Biological Rhythms; Development of the Brain
Link ID: 24060 - Posted: 09.13.2017

By Clare Wilson Have we had our first peek at the source of nightmares? When rats are given a fright while they are awake, the fear centre of their brains gets reactivated when they next go to sleep. This could explain why people who go through frightening experiences often have nightmares afterwards, says György Buzsáki of New York University. Rats store mental maps of the world they experience in their hippocampi – two curved structures in the brain. Different places are processed by distinct groups of neurons in the hippocampi that fire together in sequence as rats run around a maze, for example. Later, after exploring an environment like this, these firing sequences have been seen replaying as the animals sleep, as if dreaming of the routes they’d taken. This process is thought to allow memories to become consolidated for longer term storage, and has recently been detected in people for the first time. Buzsáki’s team wondered if such memory replay might include not just spatial information but also how the animal was feeling at the time. They tested this by giving a rat an unpleasant but harmless experience – a puff of air in the face from a computer keyboard cleaner – at a particular spot along a route. As expected, the rats learned to fear that particular place. “They slow down before the location of the air puff, then run superfast away from it,” says Buzsáki’s colleague, Gabrielle Girardeau. “If you do it in the face of a human, they don’t like it either.” © Copyright New Scientist Ltd.

Keyword: Sleep; Learning & Memory
Link ID: 24058 - Posted: 09.12.2017

By Michelle Roberts Health editor, BBC News online There is "surprisingly limited" evidence that light drinking during pregnancy poses any risk to the baby, say UK researchers. They reviewed all the available studies done on the topic since the 1950s and found no convincing proof that a drink or two a week is harmful. The Bristol University team stress this does not mean it is completely safe. They say women should avoid all alcohol throughout pregnancy "just in case", as per official guidelines. But women who have had small amounts to drink in pregnancy should be reassured that they are unlikely to have harmed their baby. The Chief Medical Officer for the UK, Prof Dame Sally Davies, updated her advice last year to advocate total abstinence. Before that, pregnant women had been told they could drink one or two units - equivalent to one or two small glasses of wine - a week. There is no proven safe amount that women can drink during pregnancy, although the risks of drinking heavily in pregnancy are well known. Getting drunk or binge drinking during pregnancy increases the risk of miscarriage and premature birth and can lead to mental and physical problems in the baby, called foetal alcohol syndrome. The risks associated with light drinking, however, are less clear. Dr Luisa Zuccolo and colleagues found 26 relevant studies on the topic. Their review found no overwhelming proof of harm - but, in seven of the studies, light drinking was associated, on average, with an 8% higher risk of having a small baby, compared with drinking no alcohol at all. The review, in BMJ Open, also notes it appeared to increase the risk of having a premature birth. © 2017 BBC.

Keyword: Development of the Brain; Drug Abuse
Link ID: 24057 - Posted: 09.12.2017

By Helen Thomson DON’T mind the gap. A woman has reached the age of 24 without anyone realising she was missing a large part of her brain. The case highlights just how adaptable the organ is. The discovery was made when the woman was admitted to the Chinese PLA General Hospital of Jinan Military Area Command in Shandong Province complaining of dizziness and nausea. She told doctors she’d had problems walking steadily for most of her life, and her mother reported that she hadn’t walked until she was 7 and that her speech only became intelligible at the age of 6. Doctors did a CAT scan and immediately identified the source of the problem – her entire cerebellum was missing (see scan, above). The space where it should be was empty of tissue. Instead it was filled with cerebrospinal fluid, which cushions the brain and provides defence against disease. The cerebellum – sometimes known as the “little brain” – is located underneath the two hemispheres. It looks different from the rest of the brain because it consists of much smaller and more compact folds of tissue. It represents about 10 per cent of the brain’s total volume but contains 50 per cent of its neurons. Although it is not unheard of to have part of your brain missing, either congenitally or from surgery, the woman joins an elite club of just nine people who are known to have lived without their entire cerebellum. A detailed description of how the disorder affects a living adult is almost non-existent, say doctors from the Chinese hospital, because most people with the condition die at a young age and the problem is only discovered on autopsy (Brain, doi.org/vh7). © Copyright New Scientist Ltd.

Keyword: Development of the Brain
Link ID: 24056 - Posted: 09.12.2017

Laura Sanders Peer inside the brain of someone learning. You might be lucky enough to spy a synapse pop into existence. That physical bridge between two nerve cells seals new knowledge into the brain. As new information arrives, synapses form and strengthen, while others weaken, making way for new connections. You might see more subtle changes, too, like fluctuations in the levels of signaling molecules, or even slight boosts in nerve cell activity. Over the last few decades, scientists have zoomed in on these microscopic changes that happen as the brain learns. And while that detailed scrutiny has revealed a lot about the synapses that wire our brains, it isn’t enough. Neuroscientists still lack a complete picture of how the brain learns. They may have been looking too closely. When it comes to the neuroscience of learning, zeroing in on synapse action misses the forest for the trees. A new, zoomed-out approach attempts to make sense of the large-scale changes that enable learning. By studying the shifting interactions between many different brain regions over time, scientists are beginning to grasp how the brain takes in new information and holds onto it. These kinds of studies rely on powerful math. Brain scientists are co-opting approaches developed in other network-based sciences, borrowing tools that reveal in precise, numerical terms the shape and function of the neural pathways that shift as human brains learn. © Society for Science & the Public 2000 - 2017.

Keyword: Learning & Memory
Link ID: 24041 - Posted: 09.06.2017

Laurel Hamers Zika’s damaging neurological effects might someday be enlisted for good — to treat brain cancer. In human cells and in mice, the virus infected and killed the stem cells that become a glioblastoma, an aggressive brain tumor, but left healthy brain cells alone. Jeremy Rich, a regenerative medicine scientist at the University of California, San Diego, and colleagues report the findings online September 5 in the Journal of Experimental Medicine. Previous studies had shown that Zika kills stem cells that generate nerve cells in developing brains (SN: 4/2/16, p. 26). Because of similarities between those neural precursor cells and stem cells that turn into glioblastomas, Rich’s team suspected the virus might also target the cells that cause the notoriously deadly type of cancer. In the United States, about 12,000 people are expected to be diagnosed with glioblastoma in 2017. (It’s the type of cancer U.S. Senator John McCain was found to have in July.) Even with treatment, most patients live only about a year after diagnosis, and tumors frequently recur. In cultures of human cells, Zika infected glioblastoma stem cells and halted their growth, Rich and colleagues report. The virus also infected full-blown glioblastoma cells but at a lower rate, and didn’t infect normal brain tissues. Zika-infected mice with glioblastoma either saw their tumors shrink or their tumor growth slow compared with uninfected mice. The virus-infected mice lived longer, too. In one trial, almost half of the mice survived more than six weeks after being infected with Zika, while all of the uninfected mice died within two weeks of receiving a placebo. |© Society for Science & the Public 2000 - 2017. A

Keyword: Glia
Link ID: 24039 - Posted: 09.06.2017

By Michael Le Page We are still evolving – very slowly. In the 20th century, people in the UK evolved to be less likely to smoke heavily, but the effect was tiny. So claims a study of 200,000 genomes. A population can be described as evolving when the frequency of gene variants changes over time. Because most people in rich countries now live well beyond reproductive age, some argue that we have stopped evolving because natural selection has been weakened. But several recent studies claim we are still evolving, albeit slowly. Now Joseph Pickrell at Columbia University in New York and his team have analysed human genome sequences to spot gene variants that are becoming rarer. One variant, of a gene called CHRNA3, is associated with heavier smoking in those that smoke, raising their risk of a smoking-related death. Comparing people over the age of 80 with people over the age of 60, Pickrell estimates that the variant has declined by 1 per cent between generations. However, his team was not able to prove this, as they did not have any genomic data from people under the age of 40. A variant of the ApoE4 gene that is known to increase the risk of late-onset Alzheimer’s disease, as well as cardiovascular disease, may also be getting rarer. © Copyright New Scientist Ltd.

Keyword: Alzheimers; Genes & Behavior
Link ID: 24038 - Posted: 09.06.2017

Anna VlasitsAnna Vlasits A sheen is starting to appear on Rocky Blumhagen’s forehead, just below his gray hair. He’s marching in place in a starkly lit room decked out with two large flatscreens. On both of the TVs, a volcano lets off steam through wide cracks glowing with lava, their roar muffling the Andean percussion and flutes on the soundtrack. Golden coins slide across the screen. Rocky reaches out his left hand, as if to grasp a coin from midair, and one of them disappears with a brrring. “I don’t know if I can do it,” he says to a guy named Josh sitting nearby in a felt-covered lounge chair. He looks up from his iPad, watching Rocky, age 66, grab, jog, kick, and reach his way through the videogame. “Keep it up,” Josh says as the heart monitor in the corner of the screen reads 129. Rocky and research assistant Josh Volponi are technically in a lab clinic at the University of California, San Francisco, but aside from the mannequin heads studded with electrodes, the room looks more like a man cave. But here, the videogames could halt the mental decay of aging. This is the premise that the university’s new research institute, named Neuroscape, was built to test. This is Rocky’s 18th training session at Neuroscape, founded by neuroscientist Adam Gazzaley. Rocky is fit for his age—he works as a substitute yoga instructor, after retiring from careers producing radio and performing Cole Porter songs—but as he makes it to the end of the level, he looks exhausted. The game cuts to an animation of a jungle, birds chirping and light playing through the canopy as a list of his past scores pops up. This round wasn’t his best. “I haven’t been here for a week,” he says. Volponi asks him to rate his physical exertion level. Rocky gives it a 15 out of 20; Volponi marks it on the iPad. “I feel rusty,” he says, wiping his hands on his orange exercise shorts.

Keyword: Alzheimers; Learning & Memory
Link ID: 24033 - Posted: 09.04.2017

Robin McKie Science Editor People who use genetic tests to trace their ancestry only to discover that they are at risk of succumbing to an incurable illness are being left to suffer serious psychological problems. Dementia researchers say the problem is particularly acute for those found to be at risk of Alzheimer’s disease, which has no cure or effective treatment. Yet these people are stumbling upon their status inadvertently after trying to find their Viking, Asian or ancient Greek roots. “These tests have the potential to cause great distress,” said Anna Middleton, head of society and ethics research at the Wellcome Genome Campus in Cambridge. “Companies should make counselling available, before and after people take tests.” The issue is raised in a paper by Middleton and others in the journal Future Medicine. A similar warning was sounded by Louise Walker, research officer at the Alzheimer’s Society. “Everyone has a right to know about their risk if they want to, but these companies have a moral responsibility to make sure people understand the meaning and consequences of this information. Anyone considering getting genetic test results should do so with their eyes open.” Alzheimer’s is linked to the build-up in the brain of clumps of a protein called amyloid. This triggers severe memory loss, confusion and disorientation. One gene, known as ApoE, affects this process and exists in three variants: E2, E3 and E4. Those possessing the last of these face an increased chance of getting the disease in late life. © 2017 Guardian News and Media Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 24031 - Posted: 09.04.2017