Chapter 7. Life-Span Development of the Brain and Behavior
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By John Carroll, Scratch yet another Phase III Alzheimer’s drug hopeful. Merck announced late Tuesday that it is shuttering its EPOCH trial for the BACE inhibitor verubecestat in mild-to-moderate Alzheimer’s after the external data monitoring committee concluded that the drug was a bust, with “virtually” no chance of success. A separate Phase III study in prodromal patients, set to read out in two years, will continue as investigators found no signs of safety issues. This is one of Merck’s top late-stage drugs, and news of the failure drove down the pharma giant’s shares in after-market trading by 2.45%. BACE drugs essentially seek to interfere in the process that creates amyloid beta, a toxic protein often found in the brains of Alzheimer’s patients. As the top amyloid beta drugs like bapineuzumab and solanezumab — which sought to extract existing amyloid beta loads — ground their way to repeated failures, developers in the field turned increasingly to BACE therapies as an alternative mechanism that could provide the key to slowing this disease down. Merck’s effort was the most advanced in the pipeline, but Eli Lilly and others are still in hot pursuit with their own persistent BACE efforts. Teams from Biogen/Eisai and Novartis/Amgen are also beavering away on BACE. “Alzheimer’s disease is one of the most pressing and daunting medical issues of our time, with inherent, substantial challenges to developing an effective disease-modifying therapy for people with mild-to-moderate disease. Studies such as EPOCH are critical, and we are indebted to the patients in this study and their caregivers,” said Dr. Roger M. Perlmutter, president, Merck Research Laboratories. © 2017 American Association for the Advancement of Science.
Link ID: 23238 - Posted: 02.16.2017
By Jesse Singal Those who advocate for sound, evidence-based research about autism are extremely alarmed about Donald Trump, and for good reason: In addition to Trump’s ties to Andrew Wakefield, the disgraced British doctor whose debunked research helped fuel the false idea of links between childhood vaccines and autism, Robert F. Kennedy Jr., a notorious anti-vaxxer himself, told reporters back in January that Trump planned to tap him as chair of a commission on “vaccine safety.” There is no question at this point that Trump has significant connections to a pseudoscientific medical movement that spreads dangerous, disproven ideas. Today, Trump gave nervous observers yet more reason to worry. It occurred at a White House event in which Trump and Secretary of Education Betsy DeVos met with a bunch of educators. Trump seemed to fixate, for a moment, on one educator named Jane (her last name is hard to make out) after she explained that she is the principal of a special education center in Virginia. The sequence starts at about 5:38 in this video: After Jane noted that many of her students have autism, Trump asked, “Have you seen a big increase in the autism, with the children?” Jane replied in the affirmative, but seemed to couch her response as being more about an increase in demand for services — she didn’t explicitly agree there’s been a big increase in the overall rate. Trump continued: “So what’s going on with autism? When you look at the tremendous increase, it’s really — it’s such an incredible — it’s really a horrible thing to watch, the tremendous amount of increase. Do you have any idea? And you’re seeing it in the school?” Jane replied — again, in a way that seems a bit noncommittal vis-à-vis Trump’s claim — that the rate of autism is something like 1-in-66 or 1-in-68 children. To which Trump responds: “Well now, it’s gotta be even lower [presumably meaning higher, rate-wise] than that, which is just amazing — well, maybe we can do something.” (Jane had the rate right, and Trump is incorrect that it has crept higher.) © 2017, New York Media LLC.
Link ID: 23233 - Posted: 02.15.2017
Ian Sample Science editor Children who are born very prematurely are at greater risk of developing mental health and social problems that can persist well into adulthood, according to one of the largest reviews of evidence. Those with an extremely low birth weight, at less than a kilogram, are more likely to have attention disorders and social difficulties as children, and feel more shyness, anxiety and depression as adults, than those born a healthy weight. The review draws on findings from 41 published studies over the past 26 years and highlights the need for doctors to follow closely how children born very prematurely fare as they become teenagers and adults. “It is important that families and doctors be aware of the potential for these early-emerging mental health problems in children born at extremely low birth weight, since at least some of them endure into adulthood,” said Karen Mathewson, a psychologist at McMaster University in Ontario. Improvements in neonatal care in the past two decades mean that more children who are born very prematurely now survive. In a healthy pregnancy, a baby can reach 1kg (a little more than 2lbs) within 27 weeks, or the end of the second trimester. The study, which involves data from 13,000 children in 12 different countries, follows previous research that found a greater tendency for very low birth weight children to have lower IQs and autism and more trouble with relationships and careers as they reach adulthood and venture into the world. © 2017 Guardian News and Media Limited
Katherine Bourzac Kristopher Boesen, who broke his neck in a car accident, regained the ability to move his arms and hands after his spinal cord was injected with stem cells. Two years after having a stroke at 31, Sonia Olea Coontz remained partially paralysed on her right side. She could barely move her arm, had slurred speech and needed a wheelchair to get around. In 2013, Coontz enrolled in a small clinical trial. The day after a doctor injected stem cells around the site of her stroke, she was able to lift her arm up over her head and speak clearly. Now she no longer uses a wheelchair and, at 36, is pregnant with her first child. Coontz is one of stem-cell therapy's “miracle patients”, says Gary Steinberg, chair of neurosurgery at Stanford School of Medicine in California, and Coontz's doctor. Conventional wisdom said that her response was impossible: the neural circuits damaged by the stroke were dead. Most neuroscientists believed that the window for functional recovery extends to only six months after the injury. Stem-cell therapies have shown great promise in the repair of brain and spinal injuries in animals. But animal models often behave differently from humans — nervous-system injuries in rats, for example, heal more readily than they do in people. Clinical trial results have been mixed. Interesting signals from small trials have faded away in larger ones. There are plenty of unknowns: which stem cells are the right ones to use, what the cells are doing when they work and how soon after an injury they can be used. © 2016 Macmillan Publishers Limited,
“Bench-to-bedside” describes research that has progressed from basic science in animal models that has led to therapies used in patients. Now, a study in the journal Brain describes what could be considered a direct “aquarium-to-bedside” approach, taking a drug discovered in a genetic zebrafish model of epilepsy and testing it, with promising results, in a small number of children with the disease. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This is the first time that scientists have taken a potential therapy discovered in a fish model directly into people in a clinical trial,” said Vicky Whittemore, Ph.D., program director at the NINDS. “These findings suggest that it may be possible to treat neurological disorders caused by genetic mutations through an efficient and precision medicine-style approach.” Scott C. Baraban, Ph.D., the William K. Bowes Jr. Endowed Chair in Neuroscience Research and professor of neurological surgery at the University of California, San Francisco (UCSF), postdoctoral fellow Aliesha Griffin, Ph.D., and colleagues used a zebrafish model of Dravet syndrome to test the drug lorcaserin and found that it suppressed seizure activity in the fish. Dravet syndrome is a severe form of pediatric epilepsy characterized by frequent daily drug-resistant seizures and developmental delays. It is caused by a genetic mutation, which Dr. Baraban’s group was able to introduce into the zebrafish to cause epilepsy. Dr. Baraban and his colleague Kelly Knupp, M.D. at the University of Colorado, Denver, then tested lorcaserin in five children with Dravet syndrome. The children were resistant to other anti-epileptic drugs and participated in this study through a compassionate use, off-label program.
In a study of mice and monkeys, National Institutes of Health funded researchers showed that they could prevent and reverse some of the brain injury caused by the toxic form of a protein called tau. The results, published in Science Translational Medicine, suggest that the study of compounds, called tau antisense oligonucleotides, that are genetically engineered to block a cell’s assembly line production of tau, might be pursued as an effective treatment for a variety of disorders. Cells throughout the body normally manufacture tau proteins. In several disorders, toxic forms of tau clump together inside dying brain cells and form neurofibrillary tangles, including Alzheimer’s disease, tau-associated frontotemporal dementia, chronic traumatic encephalopathy and progressive supranuclear palsy. Currently there are no effective treatments for combating toxic tau. "This compound may literally help untangle the brain damage caused by tau,” said Timothy Miller, M.D., Ph.D., the David Clayson Professor of Neurology at Washington University, St. Louis, and the study's senior author. Antisense oligonucleotides are short sequences of DNA or RNA programmed to turn genes on or off. Led by Sarah L. DeVos, a graduate student in Dr. Miller’s lab, the researchers tested sequences designed to turn tau genes off in mice that are genetically engineered to produce abnormally high levels of a mutant form of the human protein. Tau clusters begin to appear in the brains of 6-month-old mice and accumulate with age. The mice develop neurologic problems and die earlier than control mice.
Link ID: 23205 - Posted: 02.09.2017
By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company
By CATHERINE SAINT LOUIS During her pregnancy, she never drank alcohol or had a cigarette. But nearly every day, Stacey, then 24, smoked marijuana. With her fiancé’s blessing, she began taking a few puffs in her first trimester to quell morning sickness before going to work at a sandwich shop. When sciatica made it unbearable to stand during her 12-hour shifts, she discreetly vaped marijuana oil on her lunch break. “I wouldn’t necessarily say, ‘Go smoke a pound of pot when you’re pregnant,’” said Stacey, now a stay-at-home mother in Deltona, Fla., who asked that her full name be withheld because street-bought marijuana is illegal in Florida. “In moderation, it’s O.K.” Many pregnant women, particularly younger ones, seem to agree, a recent federal survey shows. As states legalize marijuana or its medical use, expectant mothers are taking it up in increasing numbers — another example of the many ways in which acceptance of marijuana has outstripped scientific understanding of its effects on human health. Often pregnant women presume that cannabis has no consequences for developing infants. But preliminary research suggests otherwise: Marijuana’s main psychoactive ingredient — tetrahydrocannabinol, or THC — can cross the placenta to reach the fetus, experts say, potentially harming brain development, cognition and birth weight. THC can also be present in breast milk. “There is an increased perception of the safety of cannabis use, even in pregnancy, without data to say it’s actually safe,” said Dr. Torri Metz, an obstetrician at Denver Health Medical Center who specializes in high-risk pregnancies. Ten percent of her patients acknowledge recent marijuana use. © 2017 The New York Times Company
By Emma Hiolski Imagine cells that can move through your brain, hunting down cancer and destroying it before they themselves disappear without a trace. Scientists have just achieved that in mice, creating personalized tumor-homing cells from adult skin cells that can shrink brain tumors to 2% to 5% of their original size. Although the strategy has yet to be fully tested in people, the new method could one day give doctors a quick way to develop a custom treatment for aggressive cancers like glioblastoma, which kills most human patients in 12–15 months. It only took 4 days to create the tumor-homing cells for the mice. Glioblastomas are nasty: They spread roots and tendrils of cancerous cells through the brain, making them impossible to remove surgically. They, and other cancers, also exude a chemical signal that attracts stem cells—specialized cells that can produce multiple cell types in the body. Scientists think stem cells might detect tumors as a wound that needs healing and migrate to help fix the damage. But that gives scientists a secret weapon—if they can harness stem cells’ natural ability to “home” toward tumor cells, the stem cells could be manipulated to deliver cancer-killing drugs precisely where they are needed. Other research has already exploited this method using neural stem cells—which give rise to neurons and other brain cells—to hunt down brain cancer in mice and deliver tumor-eradicating drugs. But few have tried this in people, in part because getting those neural stem cells is hard, says Shawn Hingtgen, a stem cell biologist at the University of North Carolina in Chapel Hill. © 2017 American Association for the Advancement of Science.
New clinical trial results provide evidence that high-dose immunosuppressive therapy followed by transplantation of a person's own blood-forming stem cells can induce sustained remission of relapsing-remitting multiple sclerosis (MS), an autoimmune disease in which the immune system attacks the central nervous system. Five years after receiving the treatment, called high-dose immunosuppressive therapy and autologous hematopoietic cell transplant (HDIT/HCT), 69 percent of trial participants had survived without experiencing progression of disability, relapse of MS symptoms or new brain lesions. Notably, participants did not take any MS medications after receiving HDIT/HCT. Other studies have indicated that currently available MS drugs have lower success rates. The trial, called HALT-MS, was sponsored by the National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, and conducted by the NIAID-funded Immune Tolerance Network (link is external) (ITN). The researchers published three-year results from the study in December 2014, and the final five-year results appear online Feb. 1 in Neurology, the medical journal of the American Academy of Neurology. “These extended findings suggest that one-time treatment with HDIT/HCT may be substantially more effective than long-term treatment with the best available medications for people with a certain type of MS,” said NIAID Director Anthony S. Fauci, M.D. “These encouraging results support the development of a large, randomized trial to directly compare HDIT/HCT to standard of care for this often-debilitating disease.”
James Gorman What fly is famous on TV? Think corpses and detectives wanting to know how long that body has been in a storage locker or suitcase. It’s the blowfly, of course. Its larvae, a.k.a. maggots, feed on rotting flesh, which could be that spouse or business partner who got in the way. Or, in a good police procedural, both the spouse and the business partner, sent to the great beyond together for their transgressions. By seeing whether the eggs have hatched and how big the larvae are, forensic scientists can get an idea of how much time has passed since the victims met their end and began the final chapter in the way of all flesh. By the way, if you have a problem with a spouse or business partner, it’s worth keeping in mind that the flies can indeed get into a suitcase. They stick their ovipositor through the gaps in the zipper. Or the newly hatched larvae themselves can sneak through. But there are aspects of the maggot’s life that have remained somewhat obscure. Martin Hall, a forensic entomologist at the Natural History Museum in London, thought that one part of the fly’s development in particular needed further study. The maggots are a bit like caterpillars in that at a certain point in their development they wrap themselves up in a case and go through one of the most astonishing events in the natural world: metamorphosis. In 10 days, the maggot, which has no legs or eyes and is something like “an animated sock,” Dr. Hall said, turns into the extraordinarily complex blowfly. No doubt blowflies are not as appealing as butterflies to most people, but chalk that up to a human bias for pretty fluttery things that land on flowers. It’s certainly not the fly’s fault. Any close-up image of its multifaceted, jewel-like eye shows that it is marvelous in its own way, even if it does feed on the dead. Science Times © 2017 The New York Times Company
Keyword: Development of the Brain
Link ID: 23169 - Posted: 01.31.2017
By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.
By Meredith Wadman Many children with congenital heart disease (CHD)—the most common major birth defect in the United States—sustain brain damage that often leads to problems with behavior, thinking, and learning. Now, for the first time, researchers have described how the lack of brain oxygen that results from heart malformations might stunt the brains of newborns, opening avenues to potential therapies that could be used even before babies are born. The results are “incredibly exciting,” says Caitlin Rollins, a child neurologist at Boston Children’s Hospital. “This kind of study allows us to start understanding the cellular mechanisms” behind the brain damage, she says. In the future, she adds, “we might be able to alter the course of brain development” with drugs targeted at the cellular anomalies and delivered during pregnancy. CHD reduces oxygen delivery to the brain at a time when the fetus most needs it. This lack of oxygen is thought to be a primary cause of the brain aberrations, which first become visible on MRI scans in the third trimester of pregnancy. (The heart anomalies themselves are commonly identified in the second trimester, on routine ultrasound scans.) Yet until now, scientists have been unclear about the underlying cellular process causing the brain problems. So a research team led by scientists at Children’s National Health System in Washington, D.C., delivered subpar levels of oxygen to newborn piglets, whose course of brain development and whose highly evolved brain structure mirrors in many respects those of humans. © 2017 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 23150 - Posted: 01.26.2017
By Andy Coghlan NEW drug will finally cure Alzheimer’s! Sound familiar? Seemingly every other week, the results of one preliminary trial or another promise that a game-changing drug for Alzheimer’s disease is just around the corner. Check back a few months later, though, and all mention of the drug has vanished, save perhaps for a terse story about a failed trial. Almost all clinical trials of new drugs to combat Alzheimer’s fail. No drug has bucked the trend in 20 years, but you wouldn’t know it from the constant promises of a breakthrough. Last November, after the failure of a particularly high-profile trial, for some the jig was up. “There are no treatments that can slow or reverse this devastating condition,” says Bryce Vissel at the University of Technology in Sydney, Australia. “There is no question that we have to look at Alzheimer’s in a different way.” So are we heading in the right direction, or do we need to rip up all the textbooks and start over? Alzheimer’s is the most common cause of dementia, and by some metrics its prevalence is rising. Alzheimer’s Disease International estimates that in 2015, 46.8 million people worldwide had dementia, a number that is set to double every 20 years, mostly because of an increasing number of older people in developing countries like India and China, leading to a global healthcare crisis. © Copyright Reed Business Information Ltd.
Link ID: 23149 - Posted: 01.26.2017
Sarah DeVos Targeting tangles of tau protein in mice with Alzheimer’s-like symptoms has reversed their brain damage, halting memory loss and extending their lives. Clumps of two types of sticky protein build up in the brains of people with Alzheimer’s disease: beta-amyloid plaques, and tangles of tau. While many attempts to develop drugs to treat Alzheimer’s have targeted beta-amyloid, tau protein tangles have long been suspected to play a role in memory loss. “Tau is what correlates with memory problems, so one hypothesis is that lowering tau could be beneficial,” says Tim Miller of Washington University in St Louis, Missouri. Now Miller’s team has purged tau tangles from the brains of Alzheimer’s-like mice for the first time. They used fragments of RNA called antisense oligonucleotides to sabotage the gene that makes tau, preventing it from being fully translated into protein. Once a day for four weeks, the team injected the antisense treatment, named Tau-ASO12, into the fluid at the base of each mouse’s spine. The mice had been genetically engineered to make a rogue form of tau similar to what is seen in people with Alzheimer’s, predisposing the mice to developing tau-related brain problems. The drug successfully spread throughout the brain, and was linked to a reduction in levels of tau that was made. It also seemed to destroy existing tau tangles, and prevent tau from spreading around the brain in older mice. © Copyright Reed Business Information Ltd.
Link ID: 23148 - Posted: 01.26.2017
By GRETCHEN REYNOLDS Being nearsighted is far more common than it once was. The prevalence of myopia, the condition’s medical name, in Americans has soared by 66 percent since the early 1970s, according to a 2009 study by the National Eye Institute; in China and other East Asian countries, as many as 90 percent of recent high school graduates are thought to be nearsighted. Myopia results when eyeballs are longer than normal, changing the angle at which light enters the eye and therefore the ability to focus on distant objects. The disorder involves a complex interplay of genetics and environment and usually begins before adolescence, when the eye is growing, but it can worsen in early adulthood. Some experts connect the elevated rates of myopia to the many hours young people stare at computers and other screens. But a recent study published in JAMA Ophthalmology suggests that a greater factor may be a side effect of all that screen-watching — it’s keeping children inside. This new study joins a growing body of research indicating that a lack of direct sunlight may reshape the human eye and impair vision. Researchers at King’s College London, the London School of Hygiene and Tropical Medicine and other institutions gave vision exams to more than 3,100 older European men and women and interviewed them at length about their education, careers and how often they remembered being outside during various stages of their lives. This biographical information was then cross-referenced with historical data about sunlight, originally compiled for research on skin cancer and other conditions. © 2017 The New York Times Company
About 11 per cent of Canadians aged 15 to 24 experienced depression at some point in their lives, and fewer than half of them sought professional help for a mental health condition over the previous year, according to Statistics Canada. The information was released Wednesday in the agency's Health Reports, and is based on data from the 2012 Canadian Community Health Survey Mental Health. The report was based on 4,031 respondents aged 15 to 24, which when extrapolated represents more than 4.4 million young people. Canadians 15 to 24 years old had a higher rate of depression than any other age group. Suicide is the second leading cause of death (after accidents), accounting for nearly a quarter of deaths in the 15-24 category, Statistics Canada said. An estimated 14 per cent of respondents reported having had suicidal thoughts at some point in their lives. The figure includes six per cent having that thought in the past 12 months. As well, 3.5 per cent had attempted suicide, according to the data. Report author Leanne Findlay said the findings confirm people with depression or suicidal thoughts are increasingly likely to seek professional help. Young people in the study were more likely to turn to friends or family, and when they did, generally felt they received a lot or some help. Factors such as perceived ability to deal with stress and "negative social interactions" — for instance, feeling others were angry with you — were related to depression and suicidal thoughts. Symptoms of depression include feeling sad or having trouble sleeping that last two weeks or more, Findlay said. "Knowledge of these risk and protective factors may facilitate early intervention," Findlay concluded. ©2017 CBC/Radio-Canada.
By Helen Briggs BBC News Babies build knowledge about the language they hear even in the first few months of life, research shows. If you move countries and forget your birth language, you retain this hidden ability, according to a study. Dutch-speaking adults adopted from South Korea exceeded expectations at Korean pronunciation when retrained after losing their birth language. Scientists say parents should talk to babies as much as possible in early life. Dr Jiyoun Choi of Hanyang University in Seoul led the research. The study is the first to show that the early experience of adopted children in their birth language gives them an advantage decades later even if they think it is forgotten, she said. ''This finding indicates that useful language knowledge is laid down in [the] very early months of life, which can be retained without further input of the language and revealed via re-learning,'' she told BBC News. In the study, adults aged about 30 who had been adopted as babies by Dutch-speaking families were asked to pronounce Korean consonants after a short training course. Korean consonants are unlike those spoken in Dutch. The participants were compared with a group of adults who had not been exposed to the Korean language as children and then rated by native Korean speakers. Both groups performed to the same level before training, but after training the international adoptees exceeded expectations. There was no difference between children who were adopted under six months of age - before they could speak - and those who were adopted after 17 months, when they had learned to talk. This suggests that the language knowledge retained is abstract in nature, rather than dependent on the amount of experience. © 2017 BBC
By Kevin Pelphrey, In September, the Florida State University football team made a visit to a Tallahassee middle school that would become famous. At lunchtime, student-athlete Travis Rudolph noticed sixth grader Bo Paske eating alone, so he joined Bo for the meal. Bo, who has autism, often sat by himself in the lunchroom. The world took note of the athlete’s gesture after his mother’s Facebook post about it went viral. “This is one day I didn’t have to worry if my sweet boy ate lunch alone, because he sat across from someone who is a hero in many eyes,” she wrote. This story touched people because it calls to mind something universal: the sting of social exclusion. We have all known children who often eat, or play, alone. And all of us have felt left out at one time or another. But although this experience may be universal, a new generation of children is experiencing a wave of inclusiveness. Technology of various types, often thought of as an isolating influence, can actually abet people’s good intentions or help those with autism learn to fit in. One new app called Sit With Us, invented by 16-year-old Natalie Hampton, helps vulnerable children who have difficulty finding a welcoming group in the lunchroom. Its motto is inspiring: “The first step to a warmer, more inclusive community can begin with LUNCH.” Sit With Us allows students to designate themselves as ‘ambassadors’ and to signal to anyone seeking company that they’re invited to join the ambassador’s table. © 2017 Scientific American
By JANE E. BRODY Insomnia is like a thief in the night, robbing millions — especially those older than 60 — of much-needed restorative sleep. As the king laments in Shakespeare’s “Henry IV, Part 2”: O sleep, O gentle sleep, Nature’s soft nurse, how have I frightened thee. That thou no more will weigh my eyelids down, And steep my senses in forgetfulness? The causes of insomnia are many, and they increase in number and severity as people age. Yet the problem is often overlooked during routine checkups, which not only diminishes the quality of an older person’s life but may also cause or aggravate physical and emotional disorders, including symptoms of cognitive loss. Most everyone experiences episodic insomnia, a night during which the body seems to have forgotten how to sleep a requisite number of hours, if at all. As distressing as that may seem at the time, it pales in comparison to the effects on people for whom insomnia — difficulty falling asleep, staying asleep or awakening much too early — is a nightly affair. A survey done in 1995 by researchers at the National Institute on Aging among more than 9,000 people aged 65 and older living in three communities revealed that 28 percent had problems falling asleep and 42 percent reported difficulty with both falling asleep and staying asleep. The numbers affected are likely to be much larger now that millions spend their pre-sleep hours looking at electronic screens that can disrupt the body’s biological rhythms. Insomnia, Dr. Alon Y. Avidan says, “is a symptom, not a diagnosis” that can be a clue to an underlying and often treatable health problem and, when it persists, should be taken seriously. Dr. Avidan is director of the sleep clinic at the University of California, Los Angeles, David Geffen School of Medicine. © 2017 The New York Times Company