Chapter 7. Life-Span Development of the Brain and Behavior
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Elaine Korry Efforts to protect children in foster care from being inappropriately medicated with powerful antipsychotic drugs got a big boost forward on Tuesday, when California Gov. Jerry Brown signed three bills into law designed to reform prescribing. Overprescribing of psychiatric meds for foster youth is a persistent problem nationwide, with children given the drugs at double or triple the rate of those not in foster care. In 2011, the federal Government Accounting Office found nearly 1 in 4 children in foster care was taking psychotropic medications, which include antipsychotics, antidepressants, mood stabilizers and stimulants. Hundreds of children were found to be taking five or more psychotropic medications at a time, and thousands were prescribed doses that exceeded FDA-approved guidelines. According to the report, monitoring programs fell short of guidelines established by the American Academy of Child and Adolescent Psychiatry. Many of the medications have side effects that include lethargy, weight gain, diabetes and tremors. The California legislation, which covers 63,000 children and teens in foster care, will allow public health nurses access to medical records to monitor the foster children who are prescribed psychotropic drugs; identify the group homes that rely most on these medications and potentially require them to take corrective action; and provide child welfare workers with better training and oversight tools to spot dangerous prescribing practices. © 2015 NPR
By CATHERINE SAINT LOUIS Ever since the Food and Drug Administration approved the use of the narcotic painkiller OxyContin for certain children in August, it has faced unabated criticism from lawmakers and public officials who are wrestling with devastating rates of prescription opioid abuse in their communities. Last week, Hillary Rodham Clinton brought the issue to the presidential race, calling the agency’s action “absolutely incomprehensible.” The crux of the issue is whether the agency’s approval will lead to more prescriptions for OxyContin in young patients. For years, the powerful long-acting drug has been prescribed off-label to very sick children in severe pain from cancer or spinal-fusion surgery. (Doctors can prescribe an approved drug to anyone and for any use they see fit regardless of specifications on the label.) The agency’s approval means those doctors will finally have “information about how to do it appropriately,” like dosage recommendations, said Dr. Stephen Ostroff, the agency’s acting commissioner, in an interview. “We recognize this is a very nuanced issue,” said Dr. Ostroff, when asked about Mrs. Clinton’s recent comments. “It needs to be understood in the context of why this was done.” Dr. Kathleen A. Neville, a pediatric oncologist at Arkansas Children’s Hospital, routinely treats children with unremitting pain caused by cancer or sickle cell anemia. Her patients are the kind the F.D.A. envisioned would benefit from OxyContin, despite its “risks of addictions, abuse and misuse” as a warning on the new label says. Dr. Neville, who said she had no financial ties to makers of painkillers, applauded the agency’s approval. “Just because OxyContin has been abused or prescribed inappropriately doesn’t mean we should deprive the children who need the drug,” she said, adding it is “our obligation to have the best level of evidence for its use in children.” © 2015 The New York Times Company
By Somer Bishop Subtle, significant. In a nutshell, these two words capture the symptoms of many girls with autism. Like many in my field, I’ve seen this subtlety firsthand. One 6-year-old girl I met several years ago seemed, at first, to have good social skills. She responded appropriately when I introduced myself, complimented my outfit, and politely answered all of my questions. It was only when I saw her again a few days later that I understood her family’s concerns: She made nearly identical overtures, as if our interaction were part of a play she had rehearsed. I also met a teenage girl with autism who was highly intelligent. Because she could not relate to the other girls at her high school, she began interacting exclusively with boys, whose social behaviors she found easier to imitate. She even went through a period of wanting to become a boy, reasoning that she might have more success navigating the social world as a male. The past several years have seen an explosion of studies aimed at backing up these one-off observations about how autism presents differently in girls than in boys. This is a welcome development, as understanding the unique presentation of autism in girls will help us to better identify and treat the disorder. Consistently recognizing autism in girls can be challenging, however. This is not only because girls with autism are as diverse as any other group of individuals with the disorder but also because most autism screening and diagnostic tools were developed based primarily on observations of behaviors in boys. © 2015 The Slate Group LLC.
By Kimberly G. Noble What if we could draw a line from key areas of a low-income child’s brain to a policy intervention that would dramatically reduce his or her chances of staying in poverty, dropping out of school and entering the criminal justice or social welfare system? Wouldn’t we want to make that policy prescription as widely available as any vaccination against childhood disease? Thanks to remarkable advances in neuroscience and the social sciences, we are closing in on this possibility. In a study published this year in Nature Neuroscience, several co-authors and I found that family income is significantly correlated with children’s brain size — specifically, the surface area of the cerebral cortex, which is the outer layer of the brain that does most of the cognitive heavy lifting. Further, we found that increases in income were associated with the greatest increases in brain surface area among the poorest children. Not surprisingly, our findings made many people uncomfortable. Some feared the study would be used to reinforce the notion that people remain in poverty because they are less capable than those with higher incomes. As neuroscientists, we interpret the results very differently. We know that the brain is most malleable in the early years of life and that experiences during that time have lifelong effects on the mind. Work by social scientists such as Sendhil Mullainathan at Harvard University and Eldar Shafir at Princeton University has shown that poverty depletes parents’ cognitive resources, leaving less capacity for making everyday decisions about parenting. These parents are also at far greater risk for depression and anxiety — poverty’s “mental tax.” All of this has important implications for children.
By Steve Mirsky Harvard neuroscientist Beth Stevens, talking about glia cells, which make up more than half the human brain. This week Stevens got a MacArthur Fellowship, the so-called genius grant, for her studies of glia. “These cells are incredibly responsive to damage or injury. They can protect our brain by, for example, clearing bacteria or debris in the brain in the case of injury and disease… “Until about 10 years ago, almost all of the research devoted to these cells was in these contexts. We discovered that there was another role for these cells in the normal healthy brain, in particular during development… “So a synapse is the junction of communication between two neurons, it’s how neurons talk to each other…we’re actually born with an excess of synaptic connections…and through this normal developmental process called pruning, a large number of these extra synapses get permanently removed or eliminated while others get strengthened and maintained. These microglial cells were in fact engulfing or eating these extra synapses. So these cells are necessary to do this and now of course we’re trying to better understand how it is that they know which synapse to prune and which synapse to leave alone. “A hallmark of many neurodegenerative diseases, including Alzheimer’s disease, is the early loss of synaptic connections or synapses…And what’s most striking about this is, it’s thought that the synapse loss happens years before you see signs of cognitive impairment or pathology. © 2015 Scientific American
By Nicholas Bakalar Breast-feeding has many benefits, but a new study suggests that it has no effect on a child’s IQ from toddlerhood through adolescence. The idea that breast-feeding might have an effect on cognition is plausible, since long-chain polyunsaturated fatty acids, which are important in neurological development, are more plentiful in breast-fed babies. British researchers studied 11,582 children born between 1994 and 1996. About two-thirds were breast-fed, for an average of four months. They followed them through age 16 and administered nine intelligence tests at regular intervals over the years. The study is in PLOS One. After controlling for parental education, maternal age, socioeconomic status and other variables, they found that girls who had been breast-fed had a weak but statistically insignificant advantage in early life over those who had not been, but the effect was not apparent in boys. Breast-feeding was not associated with gains in IQ through adolescence for either girls or boys. The lead author, Sophie von Stumm, a senior lecturer in psychology at Goldsmiths University of London, said that mothers who do not breast-feed are sometimes criticized. “It’s almost an accusation these days,” she said, “that you’re purposely harming your child. That’s not the case, and it’s not helpful for new mothers. Kids do lots of things that have an influence on IQ. Breast-feeding has no effect that can be distinguished from family background or socioeconomic status.” © 2015 The New York Times Company
Allison Aubrey We might not be able to remember every stressful episode of our childhood. But the emotional upheaval we experience as kids — whether it's the loss of a loved one, the chronic stress of economic insecurity, or social interactions that leave us tearful or anxious — may have a lifelong impact on our health. In fact, a study published this week in the Journal of the American College of Cardiology indicates that emotional distress during childhood — even in the absence of high stress during adult years — can increase the risk of developing heart disease and metabolic disorders such as diabetes in adulthood. Robert Wood Johnson Foundation Shots - Health News Take The ACE Quiz — And Learn What It Does And Doesn't Mean "We know that the childhood period is really important for setting up trajectories of health and well-being," explains Ashley Winning, an author of the study and postdoctoral research fellow in social and behavioral sciences at the Harvard T.H. Chan School of Public Health. To assess the connection between childhood stress and the risk of disease, Winning and her colleagues analyzed data from the 1958 British Birth Cohort Study, a long-running study that documented the diets, habits and emotional health of thousands of British children born during the same week that year. As the children entered school, the classroom became the laboratory for observation. © 2015 NPR
By Nicholas Bakalar Agitation and aggression are common in Alzheimer’s patients, and there is no known safe and effective treatment. Now researchers report that a combination drug already in use for treating certain neurological problems may be a better remedy. Dextromethorphan is a cough suppressant commonly found in over-the-counter cough medicines, and quinidine is a drug used to control heart rhythm disorders. In combination, they are used to treat certain neurological disorders involving involuntary movement of the facial muscles. The scientists randomized 152 Alzheimer’s patients to a 10-week course of dextromethorphan-quinidine and 127 to placebo. Researchers then rated them using a well-validated scale that measures aggression and agitation. The study is in the Sept. 22 issue of JAMA. Aggression scores declined to 3.8 from 7.1 in the dextromethorphan-quinidine group and to 5.3 from 7.0 in those who took a placebo. Then the researchers re-randomized those who did not respond to placebo to receive either drugs or placebo, and found similar encouraging results for the drug combination. “Fifty-five percent of the people who were on drugs had a 50 percent reduction in their agitation,” said the lead author, Dr. Jeffrey L. Cummings, director of the Cleveland Clinic Lou Ruvo Center for Brain Health. “That’s a lot when a patient is striking and hitting and cussing. There are no currently approved treatments for agitation, and we’re very enthusiastic about this finding.” © 2015 The New York Times Company
By Kelly Servick Children born to obese mothers arrive already predisposed to obesity and other health problems themselves. Exactly what happens in the uterus to transmit this risk still isn’t clear, but a new study on mice points to the placenta as a key actor. The study shows that a hormone acting on the placenta can protect the offspring of obese mice from being born overweight. It suggests ways to break the cycle of obesity in humans—although other researchers caution there's a long way to go. Researchers discovered decades ago that conditions in the uterus can “program” a fetus to be more susceptible to certain health problems. People conceived during the 1944 famine in the Netherlands, for example, suffered higher rates of cardiovascular disease, diabetes, cancer, and other problems later in life. Recent animal studies suggest that malnourishment in the womb changes the expression of DNA in ways that can be passed down for generations. But researchers are now increasingly concerned with the opposite problem. Obese women tend to give birth to larger babies with more body fat, and these children are more likely to develop metabolic syndrome—the cluster of conditions including obesity and high blood sugar that can lead to diabetes and heart disease. To probe the roots of fetal “overgrowth,” developmental biologists at the University of Colorado, Denver, looked to the placenta—the whoopee cushion–shaped organ wedged between the fetus and the wall of the uterus, where branching arteries from the umbilical cord take up oxygen and nutrients from the mother’s blood vessels. The placenta “has always been viewed as a passive organ—whatever happens to the mother is translated toward the fetus,” says lead author Irving Aye, now at the University of Cambridge in the United Kingdom. However, recent research has shown that the placenta is less an indiscriminate drainpipe than a subtle gatekeeper. © 2015 American Association for the Advancement of Science.
By Judith Berck The 73-year-old widow came to see Dr. David Goodman, an assistant professor in the psychiatry and behavioral sciences department at Johns Hopkins School of Medicine, after her daughter had urged her to “see somebody” for her increasing forgetfulness. She was often losing her pocketbook and keys and had trouble following conversations, and 15 minutes later couldn’t remember much of what was said. But he did not think she had early Alzheimer’s disease. The woman’s daughter and granddaughter had both been given a diagnosis of A.D.H.D. a few years earlier, and Dr. Goodman, who is also the director of a private adult A.D.H.D. clinical and research center outside of Baltimore, asked about her school days as a teenager. “She told me: ‘I would doodle because I couldn’t pay attention to the teacher, and I wouldn’t know what was going on. The teacher would move me to the front of the class,’ ” Dr. Goodman said, After interviewing her extensively, noting the presence of patterns of impairment that spanned the decades, Dr. Goodman diagnosed A.D.H.D. He prescribed Vyvanse, a short-acting stimulant of the central nervous system. A few weeks later, the difference was remarkable. “She said: ‘I’m surprised, because I’m not misplacing my keys now, and I can remember things better. My mind isn’t wandering off, and I can stay in a conversation. I can do something until I finish it,’ ” Dr. Goodman said. Once seen as a disorder affecting mainly children and young adults, attention deficit hyperactivity disorder is increasingly understood to last throughout one’s lifetime. © 2015 The New York Times Company
Linda Geddes Jack struggled in regular school. Diagnosed with dyslexia and the mathematical equivalent, dyscalculia, as well as the movement disorder dyspraxia, Jack (not his real name) often misbehaved and played the class clown. So the boy’s parents were relieved when he was offered a place at Fairley House in London, which specializes in helping children with learning difficulties. Fairley is also possibly the first school in the world to have offered pupils the chance to undergo electrical brain stimulation. The stimulation was done as part of an experiment in which twelve eight- to ten-year-olds, including Jack, wore an electrode-equipped cap while they played a video game. Neuroscientist Roi Cohen Kadosh of the University of Oxford, UK, who led the pilot study in 2013, is one of a handful of researchers across the world who are investigating whether small, specific areas of a child’s brain can be safely stimulated to overcome learning difficulties. “It would be great to be able to understand how to deliver effective doses of brain stimulation to kids’ brains, so that we can get ahead of developmental conditions before they really start to hold children back in their learning,” says psychologist Nick Davis of Swansea University, UK. The idea of using magnets or electric currents to treat psychiatric or learning disorders — or just to enhance cognition — has generated a flurry of excitement over the past ten years. The technique is thought to work by activating neural circuits or by making it easier for neurons to fire. The research is still in its infancy, but at least 10,000 adults have undergone such stimulation, and it seems to be safe — at least in the short term. One version of the technology, called transcranial magnetic stimulation (TMS), has been approved by the US Food and Drug Administration to treat migraine and depression in adults. © 2015 Nature Publishing Group,
Claudia Dreifus Cornelia Bargmann, a neurobiologist at Rockefeller University in New York, studies how genes interact with neurons to create behavior. Two years ago, President Obama named Dr. Bargmann, who is known as Cori, a co-chairwoman of the advisory commission for the Brain Initiative, which he has described as “giving scientists the tools they need to get a dynamic picture of the brain in action.” I spoke with Dr. Bargmann, 53, for two hours at the Manhattan apartment she shares with her husband, Dr. Richard Axel, a neuroscientist at Columbia University. Our interview has been edited and condensed. Q. As an M.I.T. graduate student, you made a discovery that ultimately led to the breast cancer drug Herceptin. How did it happen? A. What I did was discover a mutated gene that triggered an obscure cancer in rats. Afterwards, it was discovered — by others — that this same gene is also altered in human breast cancers. Since our work in the rat cancer showed that the immune system could attack the product of this gene, Genentech developed a way to deploy the immune system. That’s Herceptin. It is an antibody against the gene that sits on the surface of a cancer cell. It can attack the cancer cell growing because of that gene. Currently, you spend your time trying to understand the nervous system of a tiny worm, C. elegans. Why do you study this worm? Well, the reason is this: Understanding the human brain is a great and complex problem. To solve the brain’s mysteries, you often have to break a problem down to a simpler form. Your brain has 86 billion nerve cells, and in any mental process, millions of them are engaged. Information is sweeping across these millions of neurons. With present technology, it’s impossible to study that process at the level of detail and speed you would want. © 2015 The New York Times Company
by Laura Sanders Like every other person who carries around a smartphone, I take a lot of pictures, mostly of my kids. I thought I was bad with a few thousand snaps filling my phone’s memory. But then I talked to MIT researcher Deb Roy. For three years, Roy and a small group of researchers recorded every waking moment of Roy’s son’s life at home, amassing over 200,000 hours of video and audio recordings. Roy’s intention wasn’t to prove he was the proudest parent of all time. Instead, he wanted to study how babies learn to say words. As a communication and machine learning expert, Roy and his wife Rupal Patel, also a speech researcher, recognized that having a child would be a golden research opportunity. The idea to amass this gigantic dataset “was kicking around and something we thought about for years,” Roy says. So after a pregnancy announcement and lots of talking and planning and “fascinating conversations” with the university administration in charge of approving human experiments, the researchers decided to go for it. To the delight of his parents, a baby boy arrived in 2005. When Roy and Patel brought their newborn home, the happy family was greeted by 11 cameras and 14 microphones, tucked up into the ceiling. From that point on, cameras rolled whenever the baby was awake. © Society for Science & the Public 2000 - 2015
Steve Connor A painkiller widely used to treat rheumatoid arthritis has been shown to reverse the symptoms of dementia in the brains of laboratory mice, raising hope that there may soon be an effective treatment for Alzheimer’s disease, scientists have said. The drug, salsalate, is a licensed pain killer but in mice with a form of dementia similar to Alzheimer’s it reversed the changes to a key protein in the brain that builds up in patients with the debilitating neurological disease, they found. The researchers said it is the first time any drug has been shown to have an effect on the “tau” protein that accumulates in the brain of people with Alzheimer’s and a range of similar dementias known as “tauopathies”. It could lead to an effective therapy even for patients in the later stages of disease, the researchers said. “We identified for the first time a pharmacological approach that reverses all aspects of tau toxicity," said Li Gan, PhD of the Gladstone Institutes, a non-profit research organisation affiliated with the University of California, San Francisco. “Remarkably, the profound protective effects of salsalate were achieved even though it was administered after disease onset, indicating that it may be an effective treatment option,” said Dr Gan a senior co-author of the study published in the journal Nature Medicine. As many as 800,000 people in Britain are already affected by Alzheimer’s disease and a new study has suggested that as many as one in three babies born this year will get dementia in their lifetime, largely as a result of people living longer. Age is the biggest risk factor for the disease. © independent.co.uk
Link ID: 21428 - Posted: 09.22.2015
By John Pavlus The “brain in a vat” has long been a staple of philosophical thought experiments and science fiction. Now scientists are one step closer to creating the real thing, which could enable groundbreaking experiments of a much more empirical kind. Research teams at Stanford University and the RIKEN Center for Developmental Biology in Japan have each discovered methods for coaxing human stem cells to form three-dimensional neural structures that display activity associated with that of an adult brain. By applying a variety of chemical growth factors, the RIKEN researchers transformed human embryonic stem cells into neurons that self-organized in patterns unique to the cerebellum, a region of the brain that coordinates movement. The Stanford team worked with induced pluripotent stem cells derived from skin cells and chemically nudged them to become neurons that spontaneously wired up into networks of 3-D circuits, much like the ones found in the cerebral cortex—the wrinkled gray matter of the brain that supports attention, memory and self-awareness in humans. “For years people have used mouse embryonic stem cells to generate teratomas—things that look like they could be organs,” says David Panchision, a neuroscientist at the National Institutes of Health, which supported the Stanford research. “But it's not organized and systematic, the way a developing brain needs to be to function.” In contrast, the Stanford team's neural structures not only self-assembled as cortexlike tissue, the neurons also sent signals to one another in coordinated patterns—just as they would in a brain. The cerebellar tissue generated by the Japanese scientists did, too. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 21427 - Posted: 09.21.2015
Mo Costandi The human brain is often said to be the most complex object in the known universe, and there’s good reason to believe that this old cliché is true. Even the apparently simple task of compiling a census of the different types of cells it contains has proven to be extremely difficult. Researchers still can’t agree on the best way to classify the numerous sub-types of neurons, and different methods produce different results, so estimates range from several hundred to over a thousand. Basket cells illustrate this neuronal identity crisis perfectly. They are currently sub-divided into multiple different types, according to their shape, electrical properties, and molecular profiles. After nearly ten years of detective work, researchers at King’s College London now reveal them to be masters of disguise. In a surprising new study, they show that these cells can dynamically switch from one identity to another in response to neuronal network activity. Basket cells are a type of interneuron, which are found scattered throughout the cerebral cortex, hippocampus, and cerebellum, and make up about 5% of the total number of cells in these brain regions. They form local circuits with each other and with pyramidal neurons, the much larger and more numerous cells that transmit information to distant parts of the brain, and synthesize the inhibitory neurotransmitter GABA, which dampens pyramidal cell activity when released. These enigmatic cells are thought to exist in more than twenty different types, the best known being the fast-spiking ones, which respond rapidly to incoming signals, and slower ones, which respond after a delay. During brain development, immature forms of all types of basket cells are created in a structure called the medial ganglionic eminence, along with various other types of brain cells. They then migrate into the developing cerebral cortex, before going on to form synaptic connections with other cells. © 2015 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 21423 - Posted: 09.20.2015
By BENEDICT CAREY Fourteen years ago, a leading drug maker published a study showing that the antidepressant Paxil was safe and effective for teenagers. On Wednesday, a major medical journal posted a new analysis of the same data concluding that the opposite is true. That study — featured prominently by the journal BMJ — is a clear break from scientific custom and reflects a new era in scientific publishing, some experts said, opening the way for journals to post multiple interpretations of the same experiment. It comes at a time of self-examination across science — retractions are at an all-time high; recent cases of fraud have shaken fields as diverse as anesthesia and political science; and earlier this month researchers reported that less than half of a sample of psychology papers held up. “This paper is alarming, but its existence is a good thing,” said Brian Nosek, a professor of psychology at the University of Virginia, who was not involved in either the original study or the reanalysis. “It signals that the community is waking up, checking its work and doing what science is supposed to do — self-correct.” The authors of the reanalysis said that many clinical studies had some of the same issues as the original Paxil study, and that data should be made freely available across clinical medicine, so that multiple parties could analyze them. The dispute itself is a long-running one: Questions surrounding the 2001 study played a central role in the so-called antidepressant wars of the early 2000s, which led to strong warnings on the labels of Paxil and similar drugs citing the potential suicide risk for children, adolescents and young adults. The drugs are considered beneficial and less risky for many adults over 25 with depression. © 2015 The New York Times Company
Nancy Shute There have been suggestions that low levels of vitamin D might be a factor in cognitive decline and Alzheimer's disease, but there's no proof that the lack of D is actually causing the problems. A study published Monday doesn't prove that link, but it does find that people with low levels of vitamin D lost key thinking skills more quickly than people with enough. The study is notable because of the diversity of the participants: 62 percent were women, 30 percent were African-American, 25 percent Hispanic and 41 percent white. Most earlier studies looking at cognitive decline and vitamin D were in white people. The participants lived in California's Sacramento Valley and were mostly in their 70s when they entered the study. The researchers followed up with them for about five years, having them take annual neurological exams and neuropsychological testing at the University of California, Davis, Alzheimer's Disease Center. Most of the 382 people in the study were low on vitamin D, tested by measuring 25-hydroxyvitamin D in the blood. One-quarter of the participants were deficient in vitamin D, and 35 percent had levels deemed insufficient. That's not a surprise — most older people are below the "adequate" level of 20 to less than 50 ng/ml, often because they're not outside much. And most of the people in the study weren't getting the recommended three servings of dairy foods daily that could help. © 2015 NPR
By CLYDE HABERMAN Perhaps no crime staggers the mind, or turns the stomach, more than the murder of a baby, and so it is not a surprise when law enforcement comes down hard on the presumed killers. Often enough, these are men and women accused of having succumbed to sudden rage or simmering frustration and literally shaken the life out of a helpless infant who would not stop crying or would not fall asleep. Shaken baby syndrome has been a recognized diagnosis for several decades, though many medical professionals now prefer the term abusive head trauma. It is defined by a constellation of symptoms known as the triad: brain swelling, bleeding on the surface of the brain and bleeding behind the eyes. For years, those three symptoms by themselves were uniformly accepted as evidence that a crime had been committed, even in the absence of bruises, broken bones or other signs of abuse. While many doctors, maybe most, still swear by the diagnosis, a growing number have lost faith. Not that they doubt that some babies have been abused. But these skeptics assert that factors other than shaking, and having nothing to do with criminal behavior, may sometimes explain the triad. Has the syndrome been diagnosed too liberally? Are some innocent parents and other caretakers being wrongly sent to prison? Those questions, at the complex intersection of medicine and the law, can stir strong emotions among doctors, parents and prosecutors. They shape this first installment in a new series of Retro Report, video documentaries that explore major news stories of the past and their enduring consequences. The video’s starting point is a Massachusetts criminal case that introduced the concept of shaken baby syndrome to many Americans: the 1997 murder trial of Louise Woodward, an 18-year-old British au pair accused of having shaken an 8-month-old boy, Matthew Eappen, so aggressively that he died. Matthew also had injuries that may have predated Ms. Woodward’s joining the Eappen family in Newton, outside Boston. The focus, however, was on the triad of symptoms. To prosecution witnesses, they proved that the baby had been shaken violently, his head hitting some hard surface. © 2015 The New York Times Company
A study suggests that a chemical in dark chocolate and red wine can slow the progression of Alzheimer’s disease. But how conclusive is the data, and does this mean we should all drink more wine? New Scientist looks at the evidence. What is resveratrol? Found in grapes, red wine and dark chocolate, many claims have been made about resveratrol. It has been touted as a potential panacea for a range of age-related disorders, including cancer, diabetes and neurological problems, but so far most of the data supporting these claims has come from lab studies and work in animals. There have been only a few, small studies in humans. How might resveratrol protect us from age-related illness? Extremely calorie-restricted diets greatly reduce age-related diseases in lab animals. This is thought to happen through the activation of a group of enzymes called sirtuins, which seem to affect gene expression and protect against the effects of stress, including a poor diet. The hope is that resveratrol activates sirtuins to get the same benefits – like preventing the onset of age-related diseases, including Alzheimer’s – without having to stick to such a low-energy diet. But some experiments have suggested slowed ageing from caloric restriction may not be down to sirtuins after all. What does the latest study show? To see if resveratrol could delay the progression of Alzheimer’s disease in people , Scott Turner at Georgetown University Medical Centre in Washington DC and his team gave 119 people with mild to moderate symptoms of the disease either a gram of synthesised resveratrol twice a day in pills for a year, or a placebo. © Copyright Reed Business Information Ltd.
Link ID: 21404 - Posted: 09.14.2015