Chapter 13. Memory, Learning, and Development
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By PAM BELLUCK The 40-year-old man showed up in Dr. Mary Malloy’s clinic with sadly disfiguring symptoms. His hands, elbows, ears and feet were blemished with protruding pustules and tuber-like welts, some so painful it was hard for him to walk. He suffered from a rare genetic condition called dysbetalipoproteinemia, which caused his cholesterol levels to soar so high that pools of fatty tissue seemed to bubble up under his skin. But there was something else about this patient. He was missing a gene that, when present in one form, greatly increases the risk of developing Alzheimer’s disease. Dr. Malloy, who co-directs the Adult Lipid Clinic at the University of California, San Francisco, and her colleagues saw an opportunity to answer an important neurological riddle: Does the absence of the gene — named apolipoprotein E, or APOE, after the protein it encodes — hurt the brain? If a person with this rare condition were found to be functioning normally, that would suggest support for a new direction in Alzheimer’s treatment. It would mean that efforts — already being explored by dementia experts — to prevent Alzheimer’s by reducing, eliminating or neutralizing the effects of the most dangerous version of APOE might succeed without causing other problems in the brain. The researchers, who reported their findings on Monday in the journal JAMA Neurology, discovered exactly that. They ran a battery of tests, including cognitive assessments, brain imaging and cerebrospinal fluid analyses. The man’s levels of beta-amyloid and tau proteins, which are markers of Alzheimer’s, gave no indication of neurological disease. His brain size was unaffected, and the white matter was healthy. His thinking and memory skills were generally normal. “This particular case tells us you can actually live without any APOE in the brain,” said Dr. Joachim Herz, a neuroscientist and molecular geneticist at University of Texas Southwestern Medical Center, who was not involved in the research. “So if they were to develop anti-APOE therapies for Alzheimer’s, we would not have to worry about serious neurological side effects.” © 2014 The New York Times Company
Link ID: 19943 - Posted: 08.12.2014
By Smitha Mundasad Health reporter, BBC News Human brains grow most rapidly just after birth and reach half their adult size within three months, according to a study in JAMA Neurology. Using advanced scanning techniques, researchers found male brains grew more quickly than those of female infants. Areas involved in movement developed at the fastest pace. Those associated with memory grew more slowly. Scientists say collating this data may help them identify early signs of developmental disorders such as autism. For centuries doctors have estimated brain growth using measuring tape to chart a baby's head circumference over time. Any changes to normal growth patterns are monitored closely as they can suggest problems with development. But as head shapes vary, these tape measurements are not always accurate. Led by scientists at the University of California, researchers scanned the brains of 87 healthy babies from birth to three months. They saw the most rapid changes immediately after birth - newborn brains grew at an average rate of 1% a day. This slowed to 0.4% per day at the end of the 90-day period. Researchers say recording the normal growth trajectory of individual parts of the brain might help them better understand how early disorders arise. They found the cerebellum, an area of the brain involved in the control of movement, had the highest rate of growth - doubling in size over the 90-day period. BBC © 2014
by Aviva Rutkin What can the human brain do for a computer? There's at least one team of researchers that thinks it might have the answer. Working at IBM Research–Almaden in San Jose, California, they have just released more details of TrueNorth, a computer chip composed of one million digital "neurons". Under way for several years, the project abandons traditional computer architecture for one inspired by biological synapses and axons. The latest results, published in Science, provide a timely reminder of the promise of brain-inspired computing. The human brain still crushes any modern machines when it comes to tasks like vision or voice recognition. What's more, it manages to do so with less energy than it takes to power a light bulb. Building those qualities into a computer is an alluring prospect to many researchers, like Kwabena Boahen of Stanford University in California. "The first time I learned how computers worked, I thought it was ridiculous," he says. "I basically felt there had to be a better way." Aping the brain's structure could help us build computers that are far more powerful and efficient than today's, says TrueNorth team leader Dharmendra Modha. "We want to approximate the anatomy and physiology, the structure and dynamics of the brain, within today's silicon technology," he says. "I think that the chip and the associated ecosystem have the potential to transform science, technology, business, government and society." But how best to go about building a proper artificial brain is a matter of debate. © Copyright Reed Business Information Ltd
Link ID: 19932 - Posted: 08.09.2014
Posted by Ewen Callaway More than 130 leading population geneticists have condemned a book arguing that genetic variation between human populations could underlie global economic, political and social differences. “A Troublesome Inheritance“, by science journalist Nicholas Wade, was published in June by Penguin Press in New York. The 278-page work garnered widespread criticism, much of it from scientists, for suggesting that genetic differences (rather than culture) explain, for instance, why Western governments are more stable than those in African countries. Wade is former staff reporter and editor at the New York Times, Science and Nature. But the letter — signed by a who’s who of population genetics and human evolution researchers, and to be published in the 10 August New York Times — represents a rare unified statement from scientists in the field and includes many whose work was cited by Wade. “It’s just a measure of how unified people are in their disdain for what was done with the field,” says Michael Eisen, a geneticist at the University of California, Berkeley, who co-drafted the letter. “Wade juxtaposes an incomplete and inaccurate explanation of our research on human genetic differences with speculation that recent natural selection has led to worldwide differences in I.Q. test results, political institutions and economic development. We reject Wade’s implication that our findings substantiate his guesswork. They do not,” states the letter, which is a response to a critical review of the book published in the New York Times. “This letter is driven by politics, not science,” Wade said in a statement. “I am confident that most of the signatories have not read my book and are responding to a slanted summary devised by the organizers.” © 2014 Macmillan Publishers Limited
Keyword: Genes & Behavior
Link ID: 19931 - Posted: 08.09.2014
by Bethany Brookshire For most of us, where our birthday falls in the year doesn’t matter much in the grand scheme of things. A July baby doesn’t make more mistakes than a Christmas kid — at least, not because of their birthdays. But for neurons, birth date plays an important role in how these cells find their connections in the brain, a new study finds. Nerve cells that form early in development will make lots of connections — and lots of mistakes. Neurons formed later are much more precise in their targeting. The findings are an important clue to help scientists understand how the brain wires itself during development. And with more information on how the brain forms its network, scientists might begin to see what happens when that network is injured or malformed. Many, many brain cells are born as the brain develops. Each one has to reach out and make connections, sometimes to other cells around them and sometimes to other regions of the brain. To do this, these nerve cells send out axons, long, incredibly thin projections that reach out to other regions. How mammalian axons end up at their final destination in the growing brain remains a mystery. To find out how developing brains get wired up, Jessica Osterhout and colleagues at the University of California, San Diego and colleagues started in the eye. They looked at retinal ganglion cells, neurons that connect the brain and the eye. “It’s easy to access,” explains Andrew Huberman, a neuroscientist at UC San Diego and an author on the paper. “Your retina is basically part of the central nervous system that got squeezed into your eye during development.” Retinal ganglion cells all have the same function: To convey visual information from the eyes to the brain. But they are not all the same. © Society for Science & the Public 2000 - 2013
Ian Sample, science editor Stroke patients who took part in a small pilot study of a stem cell therapy have shown tentative signs of recovery six months after receiving the treatment. Doctors said the condition of all five patients had improved after the therapy, but that larger trials were needed to confirm whether the stem cells played any part in their progress. Scans of the patients' brains found that damage caused by the stroke had reduced over time, but similar improvements are often seen in stroke patients as part of the normal recovery process. At a six-month check-up, all of the patients fared better on standard measures of disability and impairment caused by stroke, but again their improvement may have happened with standard hospital care. The pilot study was designed to assess only the safety of the experimental therapy and with so few patients and no control group to compare them with, it is impossible to draw conclusions about the effectiveness of the treatment. Paul Bentley, a consultant neurologist at Imperial College London, said his group was applying for funding to run a more powerful randomised controlled trial on the therapy, which could see around 50 patients treated next year. "The improvements we saw in these patients are very encouraging, but it's too early to draw definitive conclusions about the effectiveness of the therapy," said Soma Banerjee, a lead author and consultant in stroke medicine at Imperial College Healthcare NHS Trust. "We need to do more tests to work out the best dose and timescale for treatment before starting larger trials." The five patients in the pilot study were treated within seven days of suffering a severe stroke. Each had a bone marrow sample taken, from which the scientists extracted stem cells that give rise to blood cells and blood vessel lining cells. These stem cells were infused into an artery that supplied blood to the brain. © 2014 Guardian News and Media Limited
by Laura Sanders In their first year, babies grow and change in all sorts of obvious and astonishing ways. As their bodies become longer, heavier and stronger, so do their brains. Between birth and a child’s first birthday, her brain nearly triples in size as torrents of newborn nerve cells create neural pathways. This incredible growth can be influenced by a baby’s early life environment, scientists have found. Tragic cases of severe neglect or abuse can throw brain development off course, resulting in lifelong impairments. But in happier circumstances, warm caregivers influence a baby’s brain, too. A new study in rats provides a glimpse of how motherly actions influence a pup’s brain. Scientists recorded electrical activity in the brains of rat pups as their mamas nursed, licked and cared for their offspring. The results, published in the July 21 Current Biology, offer a fascinating minute-to-minute look at the effects of parenting. Researchers led by Emma Sarro of New York University’s medical school implanted electrodes near six pups’ brains to record neural activity. Video cameras captured mother-pup interactions, allowing the scientists to link specific maternal behaviors to certain sorts of brain activity. Two types of brain patterns emerged: a highly alert state and a sleepier, zoned-out state, Sarro and colleagues found. Pups’ brains were alert while they were drinking milk and getting groomed by mom. Pups’ brains’ were similarly aroused when the pups were separated from their mom and siblings. Some scientists think that these bursts of brain activity help young brains form the right connections between regions. © Society for Science & the Public 2000 - 2013.
By Sandhya Somashekhar The first time Jeremy Clark met his 18-year-old client, the teenager was sitting in his vice principal’s office, the drawstrings of his black hoodie pulled tight. Jacob had recently disclosed to his friends on Facebook that he was hearing voices, and their reaction had been less than sympathetic. So Clark was relieved when a beaming Jacob showed up on time for their next meeting, at a comic book shop. As the pair bantered about “Star Wars” and a recent Captain America movie, however, Clark picked up troubling signs: Jacob said he was “detaching” from his family, often huddling alone in his room. As the visit ended, Clark gave the teen a bear hug and made a plan. “Let’s get together again next week,” he said. The visit was part of a new approach being used nationwide to find and treat teenagers and young adults with early signs of schizophrenia. The goal is to bombard them with help even before they have had a psychotic episode — a dramatic and often devastating break with reality that is a telltale sign of the disease. The program involves an intensive two-year course of socialization, family therapy, job and school assistance, and, in some cases, antipsychotic medication. What makes the treatment unique is that it focuses deeply on family relationships, and occurs early in the disease, often before a diagnosis. So far, the results have been striking: In Portland, Maine, where the treatment was pioneered, the rate of hospitalizations for first psychotic episodes fell by 34 percent over a six-year period, according to a March study. And just last month, a peer-reviewed study published in the journal Schizophrenia Bulletin found that young people undergoing the treatment at six sites around the country were more likely to be in school or working than adolescents who were not in the program. The research was funded by a $17 million grant from the Robert Wood Johnson Foundation.
Older people who have a severe vitamin D deficiency have an increased risk of developing dementia, a study has suggested. UK researchers, writing in Neurology, looked at about 1,650 people aged over 65. This is not the first study to suggest a link - but its authors say it is the largest and most robust. However, experts say it is still too early to say elderly people should take vitamin D as a preventative treatment. There are 800,000 people with dementia in the UK with numbers set to rise to more than one million by 2021. Vitamin D comes from foods - such as oily fish, supplements and exposing skin to sunlight. However older people's skin can be less efficient at converting sunlight into Vitamin D, making them more likely to be deficient and reliant on other sources. The international team of researchers, led by Dr David Llewellyn at the University of Exeter Medical School, followed people for six years. All were free from dementia, cardiovascular disease and stroke at the start of the study. At the end of the study they found the 1,169 with good levels of vitamin D had a one in 10 chance of developing dementia. Seventy were severely deficient - and they had around a one in five risk of dementia. 'Delay or even prevent' Dr Llewellyn said: "We expected to find an association between low vitamin D levels and the risk of dementia and Alzheimer's disease, but the results were surprising - we actually found that the association was twice as strong as we anticipated." He said further research was needed to establish if eating vitamin D rich foods such as oily fish - or taking vitamin D supplements - could "delay or even prevent" the onset of Alzheimer's disease and dementia. But Dr Llewellyn added: "We need to be cautious at this early stage and our latest results do not demonstrate that low vitamin D levels cause dementia. BBC © 2014
by Bethany Brookshire Every day sees a new research article on addiction, be it cocaine, heroin, food or porn. Each one takes a specific angle on how addiction works in the brain. Perhaps it’s a disorder of reward, with drugs hijacking a natural system that is meant to respond to food, sex and friendship. Possibly addiction is a disorder of learning, where our brains learn bad habits and responses. Maybe we should think of addiction as a combination of an environmental stimulus and vulnerable genes. Or perhaps it’s an inappropriate response to stress, where bad days trigger a relapse to the cigarette, syringe or bottle. None of these views are wrong. But none of them are complete, either. Addiction is a disorder of reward, a disorder of learning. It has genetic, epigenetic and environmental influences. It is all of that and more. Addiction is a display of the brain’s astounding ability to change — a feature called plasticity — and it showcases what we know and don’t yet know about how brains adapt to all that we throw at them. “A lot of people think addiction is what happens when someone finds a drug to be the most rewarding thing they’ve ever experienced,” says neuroscientist George Koob, director of the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Md. “But drug abuse is not just feeling good about drugs. Your brain is changed when you misuse drugs. It is changed in ways that perpetuate the problem.” The changes associated with drug use affect how addicts respond to drug cues, like the smell of a cigarette or the sight of a shot of vodka. Drug abuse also changes how other rewards, such as money or food are processed, decreasing their relative value. © Society for Science & the Public 2000 - 2013
By DOUGLAS QUENQUA A tiny part of the brain keeps track of painful experiences and helps determine how we will react to them in the future, scientists say. The findings could be a boon to depression treatments. The habenula (pronounced ha-BEN-you-la), a part of the brain less than half the size of a pea, has been shown in animal studies to activate during painful or unpleasant episodes. Using M.R.I.s to produce powerful brain scans, researchers at University College London tracked the habenulas in subjects who were hooked up to electric shock machines. The subjects were presented with a series of photographs, some of which were followed by increasingly strong shocks. Soon, when the subjects were shown pictures associated with shocks, their habenulas would light up. “The habenula seems to track the associations with electric shocks becoming stronger and stronger,” said Jonathan Roiser, a neuroscientist at the college and an author of the study, published in The Proceedings of the National Academy of Sciences. The habenula appeared to have an effect on motivation, too. The subjects had been asked to occasionally press a button, just to show they were awake. They were much slower to do so when their habenula was active. In fact, the more slowly they responded, the more reliably their habenulas tracked associations with shocks. In animals, the habenula has been shown to suppress production of dopamine, a chemical that drives motivation. Perhaps, the researchers say, an overactive habenula can cause the feelings of impending doom and low motivation common in people with depression. © 2014 The New York Times Company
By Emily Underwood Old age may make us wiser, but it rarely makes us quicker. In addition to slowing down physically, most people lose points on intelligence tests as they enter their golden years. Now, new research suggests the loss of certain types of cognitive skills with age may stem from problems with basic sensory tasks, such as making quick judgments based on visual information. Although there’s no clear causal link between the two types of thinking yet, the new work could provide a simple, affordable way to track mental decline in senior citizens, scientists say. Since the 1970s, researchers who study intelligence have hypothesized that smartness, as measured on standard IQ tests, may hinge on the ability to quickly and efficiently sample sensory information from the environment, says Stuart Ritchie, a psychologist at the University of Edinburgh in the United Kingdom. Today it’s well known that people who score high on such tests do, indeed, tend to process such information more quickly than those who do poorly, but it’s not clear how these measures change with age, Ritchie says. Studying older people over time can be challenging given their uncertain health, but Ritchie and his colleagues had an unusual resource in the Lothian Birth Cohort, a group of people born in 1936 whose mental function has been periodically tested by the Scottish government since 1947—their first IQ test was at age 11. After recruiting more than 600 cohort members for their study, Ritchie and colleagues tracked their scores on a simple visual task three times over 10 years, repeating the test at the mean ages of 70, 73, and 76. © 2014 American Association for the Advancement of Science
Claudia M. Gold In the course of working on my new book about listening to parents and children, I have had the pleasure of immersing myself in the writing of D.W. Winnicott, pediatrician turned psychoanalyst. Winnicott's professional life included both caring for countless young children and families as a pediatrician, and psychoanalytic practice, where his adult patients "regressed to dependence," giving him an opportunity to interact with their infantile qualities, but with adult capacities for communication. This combination of experiences gave him a unique vantage point from which to make his many brilliant observations about children and the nature of the parent-child relationship. A recent New York Times Magazine article on autism prompted me to share his words of wisdom on the subject, which, though written in 1966, still have relevance today. The following is from a collection of papers, Thinking About Children: From my point of view the invention of the term autism was a mixed blessing...I would like to say that once this term has been invented and applied, the stage was set for something which is slightly false, i.e. the discovery of a disease…Pediatricians and physically minded doctors as a whole like to think in terms of diseases which gives a tidy look to the textbooks... The unfortunate thing is that in matters psychological things are not like that. Winnicott implores the reader to instead understand the child in relational and developmental context. He writes: The subject quickly becomes one not of autism and not of the early roots of a disorder that might develop in to autism, but rather one of the whole story of human emotional development and the relationship of the process in the individual child to the environmental provision which may or may not in any one particular case facilitate the maturational process. ©2014 Boston Globe Media Partners, LLC
Link ID: 19915 - Posted: 08.05.2014
By RUTH PADAWER At first, everything about L.'s baby boy seemed normal. He met every developmental milestone and delighted in every discovery. But at around 12 months, B. seemed to regress, and by age 2, he had fully retreated into his own world. He no longer made eye contact, no longer seemed to hear, no longer seemed to understand the random words he sometimes spoke. His easygoing manner gave way to tantrums and head-banging. “He had been this happy, happy little guy,” L. said. “All of a sudden, he was just fading away, falling apart. I can’t even describe my sadness. It was unbearable.” More than anything in the world, L. wanted her warm and exuberant boy back. A few months later, B. received a diagnosis of autism. His parents were devastated. Soon after, L. attended a conference in Newport, R.I., filled with autism clinicians, researchers and a few desperate parents. At lunch, L. (who asked me to use initials to protect her son’s privacy) sat across from a woman named Jackie, who recounted the disappearance of her own boy. She said the speech therapist had waved it off, blaming ear infections and predicting that Jackie’s son, Matthew, would be fine. She was wrong. Within months, Matthew acknowledged no one, not even his parents. The last word he had was “Mama,” and by the time Jackie met L., even that was gone. In the months and years that followed, the two women spent hours on the phone and at each other’s homes on the East Coast, sharing their fears and frustrations and swapping treatment ideas, comforted to be going through each step with someone who experienced the same terror and confusion. When I met with them in February, they told me about all the treatments they had tried in the 1990s: sensory integration, megadose vitamins, therapeutic horseback riding, a vile-tasting powder from a psychologist who claimed that supplements treated autism. None of it helped either boy. Together the women considered applied behavior analysis, or A.B.A. — a therapy, much debated at the time, that broke down every quotidian action into tiny, learnable steps, acquired through memorization and endless repetition; they rejected it, afraid it would turn their sons into robots. But just before B. turned 3, L. and her husband read a new book by a mother claiming that she used A.B.A. on her two children and that they “recovered” from autism. © 2014 The New York Times Company
Link ID: 19913 - Posted: 08.02.2014
By Fredrick Kunkle The way older people walk may provide a reliable clue about how well their brain is aging and could eventually allow doctors to determine whether they are at risk of Alzheimer’s, researchers have found. The study, involving thousands of older people in several countries, suggests that those whose walking pace begins to slow and who also have cognitive complaints are more than twice as likely to develop dementia within 12 years. The findings are among the latest attempts to find and develop affordable, inexpensive diagnostic tools to determine whether a person is at risk for dementia. Last month, researchers attending the Alzheimer’s Association International Conference in Copenhagen presented several studies focused on locating biomarkers of dementia in its earliest stages. Among other things, scientists reported a connection between dementia and sense of smell that suggested a common scratch-and-sniff test could be used to help identify onset of dementia, while other researchers suggested that eye scans could also be useful someday be able to detect Alzheimer’s. Different studies found a new abnormal protein linked to Alzheimer’s and a possible link between sleep disorders and the onset of dementia. Now, researchers at the Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center say that a simple test to measure a patient’s cognitive abilities and walking speed could provide a new diagnostic tool to identify people at risk for dementia. It could be especially important tool in low- and middle-income countries with less access to sophisticated and costly technology, the scientists said.
Link ID: 19910 - Posted: 08.02.2014
By PAULA SPAN Call me nuts, but I want to talk more about sleeping pill use. Hold your fire for a few paragraphs, please. Just a week after I posted here about medical efforts to help wean older patients off sleeping pills — causing a flurry of comments, many taking exception to the whole idea as condescending or dismissive of the miseries of insomnia — researchers at the Centers for Disease Control and Prevention and Johns Hopkins published findings that reinforce concerns about these drugs. I say “reinforce” because geriatricians and other physicians have fretted for years about the use of sedative-hypnotic medications, including benzodiazepines (like Ativan, Klonopin, Xanax and Valium) and the related “Z-drugs” (like Ambien) for treating insomnia. “I’m not comfortable writing a prescription for these medications,” said Dr. Cara Tannenbaum, the geriatrician at the University of Montreal who led the weaning study. “I haven’t prescribed a sedative-hypnotic in 15 years.” In 2013, the American Geriatrics Society put sedative-hypnotics on its first Choosing Wisely campaign list of “Five Things Physicians and Patients Should Question,” citing heightened fall and fracture risks and automobile accidents in older patients who took them. Now the C.D.C. has reported that a high number of emergency room visits are associated with psychiatric medications in general, and zolpidem — Ambien — in particular. They’re implicated in 90,000 adult E.R. visits annually because of adverse reactions, the study found; more than 19 percent of those visits result in hospital admissions. Among those taking sedatives and anxiety-reducing drugs, “a lot of visits were because people were too sleepy or hard to arouse, or confused,” said the lead author, Dr. Lee Hampton, a medical officer at the C.D.C. “And there were also a lot of falls.” © 2014 The New York Times Company
|By Annie Sneed It's easy to recall events of decades past—birthdays, high school graduations, visits to Grandma—yet who can remember being a baby? Researchers have tried for more than a century to identify the cause of “infantile amnesia.” Sigmund Freud blamed it on repression of early sexual experiences, an idea that has been discredited. More recently, researchers have attributed it to a child's lack of self-perception, language or other mental equipment required to encode memories. Neuroscientists Paul Frankland and Sheena Josselyn, both at the Hospital for Sick Children in Toronto, do not think linguistics or a sense of self offers a good explanation, either. It so happens that humans are not the only animals that experience infantile amnesia. Mice and monkeys also forget their early childhood. To account for the similarities, Frankland and Josselyn have another theory: the rapid birth of many new neurons in a young brain blocks access to old memories. In a new experiment, the scientists manipulated the rate at which hippocampal neurons grew in young and adult mice. The hippocampus is the region in the brain that records autobiographical events. The young mice with slowed neuron growth had better long-term memory. Conversely, the older mice with increased rates of neuron formation had memory loss. Based on these results, published in May in the journal Science, Frankland and Josselyn think that rapid neuron growth during early childhood disrupts the brain circuitry that stores old memories, making them inaccessible. Young children also have an underdeveloped prefrontal cortex, another region of the brain that encodes memories, so infantile amnesia may be a combination of these two factors. © 2014 Scientific American
|By Jillian Rose Lim and LiveScience People who don't get enough sleep could be increasing their risk of developing false memories, a new study finds. In the study, when researchers compared the memory of people who'd had a good night's sleep with the memory of those who hadn't slept at all, they found that, under certain conditions, sleep-deprived individuals mix fact with imagination, embellish events and even "remember" things that never actually happened. False memories occur when people's brains distort how they remember a past event — whether it's what they did after work, how a painful relationship ended or what they witnessed at a crime scene. Memory is not an exact recording of past events, said Steven Frenda, a psychology Ph.D. student at the University of California, Irvine, who was involved in the study. Rather, fresh memories are constructed each time people mentally revisit a past event. During this process, people draw from multiple sources — like what they've been told by others, what they've seen in photographs or what they know as stereotypes or expectations, Frenda said. The new findings "have implications for people's everyday lives —recalling information for an exam, or in work contexts, but also for the reliability of eyewitnesses who may have experienced periods of restricted or deprived sleep," said Frenda, who noted that chronic sleep deprivation is on the rise. In a previous study, Frenda and his colleagues observed that people with restricted sleep (less than 5 hours a night) were more likely to incorporate misinformation into their memories of certain photos, and report they had seen video footage of a news event that didn't happen. In the current study, they wanted to see how a complete lack of sleep for 24 hours could influence a person's memory. © 2014 Scientific American
By DOUGLAS QUENQUA Like Pavlov’s dogs, most organisms can learn to associate two events that usually occur together. Now, a team of researchers says they have identified a gene that enables such learning. The scientists, at the University of Tokyo, found that worms could learn to avoid unpleasant situations as long as a specific insulin receptor remained intact. Roundworms were exposed to different concentrations of salt; some received food during the initial exposure, others did not. Later, when exposed to various concentrations of salt again, the roundworms that had been fed during the first stage gravitated toward their initial salt concentrations, while those that had been starved avoided them. But the results changed when the researchers repeated the experiment using worms with a defect in a particular receptor for insulin, a protein crucial to metabolism. Those worms could not learn to avoid the salt concentrations associated with starvation. “We looked for different forms of the receptor and found that a new one, which we named DAF-2c, functions in taste-aversion learning,” said Masahiro Tomioka, a geneticist at the University of Tokyo and an author of the study, which was published in the journal Science. “It turned out that only this form of the receptor can support learning” in roundworms. While human insulin receptors bear some resemblance to those of a roundworm, more study is needed to determine if it plays a similar role in memory and decision-making, Dr. Tomioka said. But studies have suggested a link between insulin levels and Alzheimer’s disease in humans. © 2014 The New York Times Company
Sara Reardon Broad population studies are shedding light on the genetic causes of mental disorders. Researchers seeking to unpick the complex genetic basis of mental disorders such as schizophrenia have taken a huge step towards their goal. A paper1 published in Nature this week ties 108 genetic locations to schizophrenia — most for the first time. The encouraging results come on the same day as a US$650-million donation to expand research into psychiatric conditions. Philanthropist Ted Stanley gave the money to the Stanley Center for Psychiatric Research at the Broad Institute in Cambridge, Massachusetts. The institute describes the gift as the largest-ever donation for psychiatric research. “The assurance of a very long life of the centre allows us to take on ambitious long-term projects and intellectual risks,” says its director, Steven Hyman. The centre will use the money to fund genetic studies as well as investigations into the biological pathways involved in conditions such as schizophrenia, autism and bipolar disorder. The research effort will also seek better animal and cell models for mental disorders, and will investigate chemicals that might be developed into drugs. The Nature paper1 was produced by the Psychiatric Genomics Consortium (PGC) — a collaboration of more than 80 institutions, including the Broad Institute. Hundreds of researchers from the PGC pooled samples from more than 150,000 people, of whom 36,989 had been diagnosed with schizophrenia. This enormous sample size enabled them to spot 108 genetic locations, or loci, where the DNA sequence in people with schizophrenia tends to differ from the sequence in people without the disease. “This paper is in some ways proof that genomics can succeed,” Hyman says. © 2014 Nature Publishing Group