Chapter 7. Life-Span Development of the Brain and Behavior
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Ian Sample Science editor The subtle impact of genetics on the age at which people lose their virginity has been teased apart by scientists and shown to have an effect on how well people fare at school. Though mostly driven by upbringing and peer behaviour, a person’s age when they first have sex is also shaped by biological factors where genes have a role to play. Researchers found that differences in DNA could account for a quarter of the variation in the age at which people lost their virginity, with other factors, among them religious beliefs, family background and peer pressure, making up the rest. Genes influence academic ability across all subjects, latest study shows Read more “We were able to calculate for the first time that there is a heritable component to age at first sex, and the heritability is about 25%, so one quarter nature, three quarters nurture,” said John Perry, an expert in reproductive ageing and related health conditions at Cambridge University. Among 38 sections of DNA found to affect the age at which people first had sex were genes that drive reproductive biology, such as the release of sex hormones and the age of puberty. Still others were found that appear to affect behaviour, personality and appearance. A variant of one of the genes, named CADM2, linked an early start to one’s sex life with risk-taking behaviour and having a large number of children. A version of another gene, MSRA, found in people who lost their virginity later than average, was linked to irritability. © 2016 Guardian News and Media Limited
Scientists believe injections of a natural protein may lessen the symptoms and progress of Alzheimer's dementia after promising early trials in mice. The treatment - IL 33 - appeared to improve memory and help clear and prevent brain deposits similar to those seen in people with Alzheimer's. Tentative human studies of the treatment will soon begin, but experts say it will take many years to know if it could help patients in real life. The work is published in PNAS journal. Interleukin 33, or IL 33 for short, is made by the body as part of its immune defence against infection and disease, particularly within the brain and spinal cord. And patients with Alzheimer's have been found to have lower amounts of IL 33 in their brains than healthy adults. The researchers from the University of Glasgow and the Hong Kong University of Science and Technology tested what effect a boost of IL 33 might have on mice bred to have brain changes akin to Alzheimer's. The rodents rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week of having the injections. Prof Eddy Liew, who led the work at the University of Glasgow, is excited but cautious about his findings. "Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done." © 2016 BBC.
Link ID: 22115 - Posted: 04.19.2016
For the first time, scientists have scanned the brains of subjects taking LSD, and found that the LSD state mimics that of infants. NPR's Rachel Martin speaks with researcher Robin Carhart-Harris. RACHEL MARTIN, HOST: Picture yourself in a boat on a river with tangerine trees and marmalade skies. Now picture yourself as a baby. You gaze up at your mother. She's got those kaleidoscope eyes. Pretty trippy, right? Turns out in a new study of brain scans, that the minds of people on LSD function in a similar way to babies' brains. Dr. Robin Carhart-Harris from Imperial College London's Center for Neuropsychopharmacology joins us from the studios of the BBC to talk about this study. So I understand this was the first time that brain scans like this have ever been done, looking specifically at the brains of people who have used LSD. How much LSD had your subjects taken? I mean, what were the prerequisites for a brain that you were going to scan? CARHART-HARRIS: Yeah, so they had to have had at least one experience with a psychedelic drug. So that includes LSD. It also includes magic mushrooms, other concoctions like ayahuasca, which is an Amazonian brew that has psychedelic properties. We gave them a moderate dose of LSD, roughly equivalent to what you might call a hit of LSD or one blotter of LSD if it was to be taken recreationally. MARTIN: So what kind of vetting did you have to do of the participants in your study because we should say different people respond to LSD in different ways? There are risks associated with this drug. CARHART-HARRIS: That's quite right. All drugs have risks, and LSD's no exception. One of the risks is that you might recruit someone who has a psychological vulnerability. So we're very, very careful when we recruit our volunteers to ensure that they have a solid mental health background. They don't have any personal or family history of any psychotic disorders - so those are things like schizophrenia. We have a psychiatrist assess them. We also evaluate their health. So they are very thoroughly screened. © 2016 npr
Dr. Perri Klass First of all, nobody takes a small child on an airplane for the fun of it. I have been there and I know. Don’t get me wrong, I’m no airplane saint; you won’t generally catch me offering to hold someone else’s kid, or making friends around the seatback. I don’t usually admit to being a pediatrician, for fear of hearing a medical saga. But I have put in my time on airplanes with my own infants and toddlers and small children, and I certainly know how it feels. Probably the best thing that can be said for traveling with young children is that it teaches you to appreciate traveling without them, however puzzling the inflight announcements, however long the delays, however tightly spaced the seats. I did enough economy-class traveling with children while my own were young that my reflexive reaction to all flight cancellations, turbulence or the moment when the person in front of me reclines the seat very suddenly, knocking my laptop closed, is now: At least I don’t have a small child with me – thank heavens. Babies do not cry on airplanes for the fun of it either. Nor do they cry, by and large, to let you know that their parents are neglectful or callous. They cry for infant versions of the same reasons that adults snap at one another about reclining seats, or elbow each other with quiet savagery over the armrest. They cry because their ears hurt and they’re being made to stay in a certain position when they don’t want to or the air smells strange and the noises are loud, or their stomachs feel upset or the day has been too long and they still aren’t there yet or they’re just plain cranky. As are we all. Crying is an evolutionary strategy to summon adult aid; over millennia, crying has probably evolved to be hard to ignore. I don’t know if it’s any comfort, but when you’re the parent with the crying baby, it doesn’t particularly help to be an expert. “I remember one flight where my daughter screamed the whole way and kept trying to get out of her seatbelt,” said my old friend, Dr. Elizabeth Barnett, a professor of pediatrics at Boston University and a travel medicine specialist. “As a parent, you feel two things — you’re in distress because you’re trying to comfort your child and not succeeding, so you feel bad for your child, and you also feel guilty because you know your child is disturbing everybody else.” © 2016 The New York Times Company
By Jordana Cepelewicz The brain relies on a system of chemical messengers, known as neurotransmitters, to carry missives from cell to cell. When all is well, these communications enable the brain to coordinate various functions, from complex thought to quick, knee-jerk reactions—but when the system is out of whack, serious disease or disorder can ensue. A team of researchers at the Technical University of Denmark (D.T.U.) and University of Oxford have for the first time identified the molecular structure of dopamine beta-hydroxylase (DBH), the enzyme that controls the conversion between dopamine and norepinephrine, two major neurotransmitters. Understanding the crystal structure of the enzyme could provide an ideal target for drug development. Dopamine and norepinephrine play key roles in many brain functions such as learning, memory, movement and the fight-or-flight response. Imbalances in the levels of these neurotransmitters—and the role DBH plays in regulating them—have been implicated in a wide range of disorders, including hypertension, congestive heart failure, anxiety, depression, post-traumatic stress disorder, Alzheimer’s, schizophrenia, Parkinson’s and even cocaine addiction. DBH has long intrigued biochemists but it has been challenging to perform the analyses needed to determine the protein’s structure. “This enzyme has been particularly difficult,” says Hans Christensen, a chemist at D.T.U. and the study’s lead researcher. “We tried many different expression systems before we finally succeeded. Now that we have the structure it is clear why—[it] is very intricate, with different parts of the enzyme interacting very tightly.” © 2016 Scientific American,
By Roni Caryn Rabin Alzheimer’s disease is a progressive brain disorder that causes dementia, destroying memory, cognitive skills, the ability to care for oneself, speak and walk, said Ruth Drew, director of family and information services at the Alzheimer’s Association. “And since the brain affects everything, Alzheimer’s ultimately affects everything,” she said, “including the ability to swallow, cough and breathe.” Once patients reach the advanced stages of Alzheimer’s, they may stop eating and become weak and susceptible to infections, said Dr. Jason Karlawish, a professor of medicine at the University of Pennsylvania. Unable to swallow or cough, they are at high risk of choking, aspirating food particles or water into the lungs and developing pneumonia, which is often the immediate cause of death, he said. “You see a general decline in the contribution the brain makes, not just in thinking, but in maintaining the body’s homeostasis,” Dr. Karlawish said. Using a feeding tube to nourish patients and hospitalizing them for infections does not significantly extend life at the advanced stages of the disease and is discouraged because it can prolong suffering with no hope of recovery, he said. Alzheimer's is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention, but that figure may underestimate the actual number of cases, Dr. Karlawish said, since some deaths may be attributed to other causes like pneumonia. © 2016 The New York Times Company
Link ID: 22071 - Posted: 04.06.2016
Mo Costandi This spectacular image – which took the best part of a year to create – shows the fine structure of a nerve terminal at high resolution, revealing, for the very first time, an intricate network of fine filaments that controls the movements of synaptic vesicles. The brain is soft and wet, with the consistency of a lump of jelly. Yet, it is the most complex and highly organized structure that we know of, containing hundreds of billions of neurons and glial cells, and something on the order of one quadrillion synaptic connections, all of which are arranged in a very specific manner. This high degree of specificity extends down to the deepest levels of brain organization. Just beneath the membrane at the nerve terminal, synaptic vesicles store neurotransmitter molecules, and await the arrival of a nervous impulse, whereupon they fuse with the membrane and release their contents into the synaptic cleft, the miniscule gap at the junction between nerve cells, and diffuse across it to bind to receptor protein molecules embedded at the surface of the partner cell. 3D model of a nerve terminal in atomic detail The process of neurotransmitter release is tightly orchestrated. Ready vesicles are ‘docked’ in the ‘active zone’ lying beneath the cell membrane, and are depleted when they fuse with the membrane, only to be replenished from a reservoir of pre-prepared vesicles located further inside the cell. Spent vesicles are quickly pulled back out of the membrane, reformed, refilled with neurotransmitter molecules, and then returned to the reservoir, so that they can be shuttled into the active zone when needed. An individual nerve cell may use up hundreds, or perhaps thousands, of vesicles every second, and so this recycling process occurs continuously to maintain the signalling between nerve cells. © 2016 Guardian News and Media Limited
Keyword: Development of the Brain
Link ID: 22067 - Posted: 04.04.2016
By DONALD G. McNEIL Jr The World Health Organization said on Thursday that there is “strong scientific consensus” that Zika virus is a cause of microcephaly, unusually small heads with brain damage in infants, as well as other neurological disorders. Yet a surge in microcephaly has been reported only in Brazil; a small increase was reported in French Polynesia, and a cluster of 32 cases is now under investigation in Colombia. For proof of the connection between infection with the virus and birth defects, scientists are waiting for the results of a large study of 5,000 pregnant women, most of them in Colombia. Women with past Zika infections will be compared with similar women without infections to see if they have more microcephalic children. The epidemic peaked in Colombia in early February, according to the W.H.O. Most of the women in the study are due to give birth in May and June. Virtually all public health agencies already believe the virus is to blame for these birth defects and are giving medical advice based on that assumption. Here are the lines of evidence they cite. As early as last August, hospitals in northeast Brazil realized that something unheard of was happening: Neonatal wards that normally saw one or two microcephalic babies a year were seeing five or more at the same time. Doctors learned from the mothers that many of them had had Zika symptoms months earlier. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22065 - Posted: 04.04.2016
The mystery is starting to untangle. It has long been known that twisted fibres of a protein called tau collect in the brain cells of people with Alzheimer’s, but their exact role in the disease is unclear. Now a study in mice has shown how tau interferes with the strengthening of connections between neurons – the key mechanism by which we form memories. In healthy cells, the tau protein helps to stabilise microtubules that act as rails for transporting materials around the cell. In people with Alzheimer’s, these proteins become toxic, but an important unanswered question is what forms of tau are toxic: the tangles may not be the whole story. In the new study, Li Gan and her colleagues at the Gladstone Institute of Neurological Disease in San Francisco found that the brains of those with Alzheimer’s have high levels of tau with a particular modification, called acetylated tau. They then looked at what acetylated tau does in a mouse model of Alzheimer’s, finding that it accumulates at synapses – the connections between neurons. When we form memories, synapses become strengthened through extra receptors inserted into the cell membranes, and this heightens their response. But acetylated tau depletes another protein called KIBRA, which is essential for this synapse-strengthening mechanism. “We’re excited because we think we now have a handle on the link between tau and memory,” says Gan. “We’re also cautious because we know this may not be the only link. It’s still early days in understanding the mechanism.” © Copyright Reed Business Information Ltd.
By Emily Underwood More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons. “It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville. Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work. What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. © 2016 American Association for the Advancement of Science
By Nicholas Bakalar Stress in childhood may be linked to hardening of the arteries in adulthood, new research suggests. Finnish researchers studied 311 children 12 to 18 years old, scoring their levels of stress according to a variety of components, including the family’s economic circumstances, the emotional environment in the home, whether parents engaged in healthy behaviors, stressful events (such as divorce, moves or death of a family member) and parental concerns about the child’s social adjustment. Using these criteria, they calculated a stress score. When the members of the group were 40 to 46 years old, they used computed tomography to measure coronary artery calcification, a marker of atherosclerosis and a risk factor for cardiovascular disease. The study, in JAMA Pediatrics, controlled for sex, cholesterol, body mass index and other factors, but still found that the higher the childhood stress score, the greater the risk for coronary artery calcification. The study is observational, and the data is based largely on parental reports, which can be biased. Still, its long follow-up time and careful control of other variables gives it considerable strength. There are plausible mechanisms for the connection, including stress-induced increases in inflammation, which in animal models have been linked to a variety of ailments. “I think that economic conditions are important here,” said the lead author, Dr. Markus Juonala, a professor of internal medicine at the University of Turku in Finland. “Public health interventions should focus on how to intervene in better ways with people with higher stress and lower socioeconomic status.” © 2016 The New York Times Company
By Matthew Hutson Earlier this month, a computer program called AlphaGo defeated a (human) world champion of the board game Go, years before most experts expected computers to rival the best flesh-and-bone players. But then last week, Microsoft was forced to silence its millennial-imitating chatbot Tay for blithely parroting Nazi propaganda and misogynistic attacks after just one day online, her failure a testimony to the often underestimated role of human sensibility in intelligent behavior. Why are we so compelled to pit human against machine, and why are we so bad at predicting the outcome? As the number of jobs susceptible to automation rises, and as Stephen Hawking, Elon Musk, and Bill Gates warn that artificial intelligence poses an existential threat to humanity, it’s natural to wonder how humans measure up to our future robot overlords. But even those tracking technology’s progress in taking on human skills have a hard time setting an accurate date for the uprising. That’s in part because one prediction strategy popular among both scientists and journalists—benchmarking the human brain with digital metrics such as bits, hertz, and million instructions per section, or MIPS—is severely misguided. And doing so could warp our expectations of what technology can do for us and to us. Since their development, digital computers have become a standard metaphor for the mind and brain. The comparison makes sense, in that brains and computers both transform input into output. Most human brains, like computers, can also manipulate abstract symbols. (Think arithmetic or language processing.) But like any metaphor, this one has limitations.
By David Z. Hambrick Nearly a century after James Truslow Adams coined the phrase, the “American dream” has become a staple of presidential campaign speeches. Kicking off her 2016 campaign, Hillary Clinton told supporters that “we need to do a better job of getting our economy growing again and producing results and renewing the American dream.” Marco Rubio lamented that “too many Americans are starting to doubt” that it is still possible to achieve the American dream, and Ted Cruz asked his supporters to “imagine a legal immigration system that welcomes and celebrates those who come to achieve the American dream.” Donald Trump claimed that “the American dream is dead” and Bernie Sanders quipped that for many “the American dream has become a nightmare.” But the American dream is not just a pie-in-the-sky notion—it’s a scientifically testable proposition. The American dream, Adams wrote, “is not a dream of motor cars and high wages merely, but a dream of social order in which each man and each woman shall be able to attain to the fullest stature of which they are innately capable…regardless of the fortuitous circumstances of birth or position.” In the parlance of behavioral genetics—the scientific study of genetic influences on individual differences in behavior—Adams’ idea was that all Americans should have an equal opportunity to realize their genetic potential. A study just published in Psychological Science by psychologists Elliot Tucker-Drob and Timothy Bates reveals that this version of the American dream is in serious trouble. Tucker-Drob and Bates set out to evaluate evidence for the influence of genetic factors on IQ-type measures (aptitude and achievement) that predict success in school, work, and everyday life. Their specific question was how the contribution of genes to these measures would compare at low versus high levels of socioeconomic status (or SES), and whether the results would differ across countries. The results reveal, ironically, that the American dream is more of a reality for other countries than it is for America: genetic influences on IQ were uniform across levels of SES in Western Europe and Australia, but, in the United States, were much higher for the rich than for the poor. © 2016 Scientific American
By Patrick Monahan Yesterday, mountaineer Richard Parks set out for Kathmandu to begin some highly unusual data-gathering. As part of Project Everest Cynllun, he will climb Mount Everest without supplemental oxygen and perform—on himself—a series of blood draws, muscle biopsies, and cognitive tests. If he makes it to the summit, these will be the highest-elevation blood and tissue samples ever collected. Damian Bailey, a physiologist at the University of South Wales, Pontypridd, in the United Kingdom and the project’s lead scientist, hopes the risky experiment will yield new information about how the human body responds to low-oxygen conditions, and how similar mechanisms might drive cognitive decline with aging. As Parks began the acclimatization process with warm-up climbs on two smaller peaks, Bailey told ScienceInsider about his ambitions for the project. This interview has been edited for clarity and brevity. Q: Parks is an extreme athlete who has climbed Everest before. What can his performance tell us about regular people? A: What we’re trying to understand is, what is it about Richard’s brain that is potentially different from other people’s brains, and can that provide us with some clues to accelerated cognitive decline, which occurs with aging [and] dementia. We know that sedentary aging is associated with a progressive decline in blood flow to the brain. … And the main challenge for sedentary aging is we have to wait so long to see the changes occurring. So this is almost a snapshot, a day in the life of a patient with cognitive decline. © 2016 American Association for the Advancement of Science.
By Esther Hsieh Spinal implants have suffered similar problems as those in the brain—they tend to abrade tissue, causing inflammation and ultimately rejection by the body. Now an interdisciplinary research collaboration based in Switzerland has made a stretchable implant that appears to solve this problem. Like Lieber's new brain implant, it matches the physical qualities of the tissue where it is embedded. The “e-dura” implant is made from a silicone rubber that has the same elasticity as dura mater, the protective skin that surrounds the spinal cord and brain, explains Stéphanie Lacour, a professor at the school of engineering at the Swiss Federal Institute of Technology in Lausanne. This feature allows the implant to mimic the movement of the surrounding tissues. Embedded in the e-dura are electrodes for stimulation and microchannels for drug therapy. Ultrathin gold wires are made with microscopic cracks that allow them to stretch. Also, the electrodes are coated with a special platinum-silicone mixture that is stretchable. In an experiment that lasted two months, the scientists found that healthy rats with an e-dura spinal implant could walk across a ladder as well as a control group with no implant. Yet rats with a traditional plastic implant (which is flexible but not stretchable) started stumbling and missing rungs a few weeks after surgery. The researchers removed the implants and found that rats with a traditional implant had flattened, damaged spinal cords—but the e-dura implants had left spinal cords intact. Cellular testing also showed a strong immune response to the traditional implant, which was minimal in rats with the e-dura implant. © 2016 Scientific American
New York's Tribeca Film Festival will not show Vaxxed, a controversial film about the MMR vaccine, its founder Robert De Niro says. As recently as Friday, Mr De Niro stood by his decision to include the film by anti-vaccination activist Andrew Wakefield in next month's festival. The link the film makes between the measles, mumps and rubella vaccine and autism has been widely discredited. "We have concerns with certain things in this film," said Mr De Niro. Mr De Niro, who has a child with autism, said he had hoped the film would provide the opportunity for discussion of the issue. But after reviewing the film with festival organisers and scientists, he said: "We do not believe it contributes to or furthers the discussion I had hoped for." Image caption Wakefield published his controversial study in 1998 Vaxxed was directed and co-written by Mr Wakefield, who described it as a "whistle-blower documentary". In a statement issued following the Tribeca Film Festival's decision, he and the film's producer Del Bigtree said that "we have just witnessed yet another example of the power of corporate interests censoring free speech, art and truth". The British doctor was the lead author of a controversial study published in 1998, which argued there might be a link between MMR and autism and bowel disease. Mr Wakefield suggested that parents should opt for single jabs against mumps, measles and rubella instead of the three-in-one vaccine. His comments and the subsequent media furore led to a sharp drop in the number of children being vaccinated against these diseases. But the study, first published in The Lancet, was later retracted by the medical journal. Mr Wakefield's research methods were subsequently investigated by the General Medical Council and he was struck off the medical register.
Link ID: 22037 - Posted: 03.28.2016
John Consentino After multiple doctors had conflicted about ADHD, I decided to move away from psychiatry and seek a neuropsychologist. I thought that autism made sense, but what ultimately led me to seek help was my focus problem. When I was 8 years old, it would take me HOURS to do homework. On Wednesdays, we got out of school at noon, and I wouldn't finish homework until about 8 p.m. No one understood why this was happening, and with all of the screaming and punishments I withstood, nothing improved. I still had GPAs near the high 90s, so all was OK, supposedly. I struggled with eye contact during that time, and this is very much apparent now. I struggled speaking to waiters/waitresses, to teachers, to family members. Speaking to members of the opposite sex was a near-impossible task. I never understood social groups. I went through all of high school in the same fashion. However, my family felt that everything was OK. I still had a mid-90 GPA, and I had made numerous friends. Unfortunately, my GPA had dropped by about 15-plus points by my senior year. I struggled badly during my first two years of college. I was constantly unhappy, and I made little to no friends. My GPA was horrid, and my time at the university was dwindling. I dropped out of school twice, and my future felt bleak. After transferring schools, I did great. So, everything was OK yet again. © 2016 npr
Link ID: 22036 - Posted: 03.28.2016
Kristin Gourlay Swaddled in soft hospital blankets, Lexi is 2 weeks old and weighs 6 pounds. She's been at Women and Infants Hospital in Providence, R.I., since she was born, and is experiencing symptoms of opioid withdrawal. Her mother took methadone to wean herself from heroin when she got pregnant, just as doctors advised. But now the hospital team has to wean newborn Lexi from the methadone. As rates of opioid addiction have continued to climb in the U.S., the number of babies born with neonatal abstinence syndrome has gone up, too — by five-fold from 2000 to 2012, according to the National Institute of Drug Abuse. It can be a painful way to enter the world, abruptly cut off from the powerful drug in the mother's system. The baby is usually born with some level of circulating opioids. As drug levels decline in the first 72 hours, various withdrawal symptoms may appear — such as trembling, vomiting, diarrhea or seizures. At some point, if symptoms mount in number or severity, doctors will begin giving medication to help ease them. The idea is to give the baby just enough opioid to reduce those symptoms, and then slowly, over days or weeks, decrease that dose to zero. A doctor comes to check on Lexi and her mother, Carrie. To protect her family's privacy, Carrie asked us not to use the family name. "So, hi, Peanut!" the doctor says to the baby. "Any concerns?" she asks Carrie. "Coming down has been catching up with her," says Carrie. © 2016 npr
Healthy body, healthy mind. Elderly people who are physically active seem to be able to stave off memory loss – but only if they start exercising before symptoms appear. At the end of a five-year period, the brains of non-exercisers look 10 years older than those who did moderate exercise. That’s what Clinton Wright at the University of Miami in Florida and his colleagues found when they followed 876 people, starting at an average age of 71, for five years. At the start of the study, each participant underwent a number of memory and cognition tests, and had the health of their brain assessed during an MRI scan. Each person was also asked how much exercise they had done in recent weeks, ranging from “no/light”, such as walking or gardening, to “moderate/heavy”, which included running and swimming. Five years later, the volunteers were called back to repeat all the tests. The participants generally performed less well than they had five years earlier. But their scores were linked to their level of exercise – those who reported no or low levels of exercise scored lower in all tests, the team found. The 10 per cent of people who said they had been engaged in moderate-to-heavy exercise not only started with higher scores in the first round of tests, but showed less of a decline five years later . Those who did little or no exercise also seemed to have worse vascular health – they had higher blood pressure, and their MRI scans showed evidence of undetected strokes. © Copyright Reed Business Information Ltd.
Nicola Davis The same genes involved in predisposing people to autism appear to influence social skills in the wider population, suggesting that the autism spectrum has no clear cut-off point, scientists have discovered. Researchers have previously shown that autism is linked not just to one or two powerful genes, but to the combined effect of many small genetic changes. The latest findings, published in Nature Genetics, suggest that social charm, empathy and the ability to make friends is about more than just practice and upbringing, but is also affected by how many of these autism risk gene variants we possess. Dr Elise Robinson, from Harvard University and a lead author on the paper, said: “This is the first study that specifically shows that ... factors that we have unambiguously associated with autism are also very clearly associated with social communication differences in the general population.” Rather than viewing a person as either having or not having such a disorder, Robinson believes our social skills are better viewed as sitting on a sliding scale across the whole population. “The primary implication is that the line at which we say people are affected or unaffected is arbitrary,” said Robinson. “There is no clear objective point either in terms of genetic risk or in terms of behavioural traits, where you can say quite simply or categorically that you’re affected or unaffected. It’s like trying to pick a point where you say someone is tall or not.” © 2016 Guardian News and Media Limited
Link ID: 22014 - Posted: 03.22.2016