Chapter 7. Life-Span Development of the Brain and Behavior
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Mr Tickle can’t bamboozle a baby. Unlike grown-ups, young infants don’t let the positioning of their bodies confuse their sense of touch. If adults who can see are touched on each hand in quick succession while their hands are crossed, they can find it hard to name which hand was touched first. Adults who have been blind from birth don’t have this difficulty, but people who become blind later in life have the same trouble as those who can still see. “That suggests that early on in life, something to do with visual experience is crucial in setting up a typical way of perceiving touch,” says Andrew Bremner at Goldsmiths, University of London. To investigate how this develops in infancy, Bremner and his colleagues compared how babies reacted to having one foot tickled. With their legs crossed over, babies aged 6 months moved the foot being tickled half of the time. But 4-month-olds did better, moving the tickled foot 70 per cent of the time – as often as they did with their legs uncrossed. The team concludes that at 4 months, babies haven’t yet learned to relate what they touch to the physical space that their body occupies. For many adults, the concept might be difficult to envision. “It’s like imagining that you feel a touch on your body, but not really knowing how that’s related to what you’re looking at,” says Bremner. “It’s almost like you have multiple sensory worlds: a visual world, an auditory world and a tactile world, which are separate and not combined in space.” © Copyright Reed Business Information Ltd.
Peter Andrey Smith Nearly a year has passed since Rebecca Knickmeyer first met the participants in her latest study on brain development. Knickmeyer, a neuroscientist at the University of North Carolina School of Medicine in Chapel Hill, expects to see how 30 newborns have grown into crawling, inquisitive one-year-olds, using a battery of behavioural and temperament tests. In one test, a child's mother might disappear from the testing suite and then reappear with a stranger. Another ratchets up the weirdness with some Halloween masks. Then, if all goes well, the kids should nap peacefully as a noisy magnetic resonance imaging machine scans their brains. “We try to be prepared for everything,” Knickmeyer says. “We know exactly what to do if kids make a break for the door.” Knickmeyer is excited to see something else from the children — their faecal microbiota, the array of bacteria, viruses and other microbes that inhabit their guts. Her project (affectionately known as 'the poop study') is part of a small but growing effort by neuroscientists to see whether the microbes that colonize the gut in infancy can alter brain development. The project comes at a crucial juncture. A growing body of data, mostly from animals raised in sterile, germ-free conditions, shows that microbes in the gut influence behaviour and can alter brain physiology and neurochemistry. © 2015 Nature Publishing Group
By Christopher Intagliata
"Babies come prepared to learn any of the world's languages." Alison Bruderer, a cognitive scientist at the University of British Columbia. "Which means no matter where they're growing up in the world, their brains are prepared to pick up the language they're listening to around them."
And listen they do. But another key factor to discerning a language’s particular sounds may be for babies to move their tongues as they listen. Bruderer and her colleagues tested that notion by sitting 24 sixth-month-olds in front of a video screen and displaying a checkerboard pattern, while they played one of two tracks: a single, repeated "D" sound in Hindi, <
Kerri Smith Scientists have discovered two extra neurons in a worm species that — they thought — already had its entire nervous system mapped. “It is a bit of a shock,” says Richard Poole, a developmental biologist at University College London (UCL), and one of the team that found the neurons by accident. The researchers call them mystery cells of the male, or MCMs, because they are found only in male nematode worms. The neurons help the worms learn when to prioritize mating over eating, revealing how a seemingly simple brain can be capable of a complex learned behaviour — and one that differs between the sexes. Caenorhabditis elegans worms are the model animal of choice for many neuroscientists, because their neural circuits are so simple that they can be mapped in full. They have two sexes: hermaphrodite and male. Hermaphrodites, the best studied, have just 302 neurons, but males have more — the MCMs raise their total to 385 neurons1. The two ‘mystery’ cells were discovered when Poole’s colleague at UCL, Arantza Barrios, was looking at the distribution of a peptide often found in neurons, called pdf-1. She saw cells light up where she thought they should not — near the worm’s nose. The neurons develop when male worms reach maturity, the researchers worked out. Their report is published in Nature1. Sex or food? © 2015 Nature Publishing Group,
By SINDYA N. BHANOO Tiny nematode worms called Caenorhabditis elegans have a peculiar reproductive story: Most females are hermaphrodites that make sperm, self-fertilize and produce more hermaphrodites. Males are few, and are known to mate with each other. Now, a new study reports that a variation in a single gene results in male worms with excretory pores that attract the sexual attentions of other males. “Other males copulate with this excretory pore, located on the neck,” said Matthew Rockman, a biologist at New York University. He and his colleagues reported their findings in the journal Current Biology. Although male worms are rare in the wild, they are easily bred in the laboratory. Researchers report that the gene variant, known as plep-1, may somehow be altering the chemical profile of the excretions in a way that makes them more attractive to other males. Copulation often does not work out well for the male that is approached, Dr. Rockman said. Males that mate with the excretory pore of another male usually leave behind a plug that weakens the worm and reduces life expectancy. Hermaphrodites with the variation of the same gene also have a lower life expectancy and do not reproduce as well. Next, the researchers want to learn what it is about a mutation in the plep-1 gene that makes males attractive to other males. © 2015 The New York Times Company
Ed Yong This week, a team from the University of California, Los Angeles claimed to have found several epigenetic marks—chemical modifications of DNA that don’t change the underlying sequence—that are associated with homosexuality in men. Postdoc Tuck Ngun presented the results yesterday at the American Society of Human Genetics 2015 conference. Nature News were among the first to break the story based on a press release issued by the conference organisers. Others quickly followed suit. “Have They Found The Gay Gene?” said the front page of Metro, a London paper, on Friday morning. Meanwhile, the mood at the conference has been decidedly less complimentary, with several geneticists criticizing the methods presented in the talk, the validity of the results, and the coverage in the press. Ngun’s study was based on 37 pairs of identical male twins who were discordant—that is, one twin in each pair was gay, while the other was straight—and 10 pairs who were both gay. He analysed 140,000 regions in the genomes of the twins and looked for methylation marks—chemical Post-It notes that dictate when and where genes are activated. He whittled these down to around 6,000 regions of interest, and then built a computer model that would use data from these regions to classify people based on their sexual orientation. The best model used just five of the methylation marks, and correctly classified the twins 67 percent of the time. “To our knowledge, this is the first example of a biomarker-based predictive model for sexual orientation,” Ngun wrote in his abstract. The problems begin with the size of the study, which is tiny. The field of epigenetics is littered with the corpses of statistically underpowered studies like these, which simply lack the numbers to produce reliable, reproducible results.
By ANDREW SOLOMON INEXPLICABLE violence is the hardest kind to accept. The human wish to insert logic where there is none often drives bystanders to psychic violence of their own. This happened again last week, after it was reported that the shooter at Umpqua Community College in Oregon, Christopher Harper-Mercer, who killed nine people and injured several others, may have been autistic. Although there is no established connection between autism and murder, some eagerly leapt to causality and scapegoating. The killer’s “diagnosis” was based primarily on posts on Yahoo made over the last decade by his mother, Laurel Harper, in which she characterized both herself and her son as having Asperger’s syndrome — a category no longer in medical use that describes autistic people with advanced verbal skills. Mr. Harper-Mercer attended a school that caters to children with special needs, including autism. While Ms. Harper is not a doctor, her descriptions of her son across his childhood are consistent with the syndrome. A Facebook page called “Families Against Autistic Shooters” ranted about “the soulless, dead eyes of autistic children,” and characterized them as “cold, calculating killing machines with no regard for human life!” Its author announced: “What do all shooters over the last few years have in common? A lack of empathy and compassion due to Autism!” If Mr. Harper-Mercer were rumored to have been diabetic or afflicted with male-pattern baldness, no such “explanations” of his behavior would have surfaced. But despite a huge increase in awareness of autism among the public, those with the condition are often subject to this type of disparagement. This was evident in both the Facebook page and the response to it by Facebook’s management, who, despite the site’s anti-bullying policy, initially refused to remove it on grounds that it did not target named individuals. “Families Against Autistic Shooters” remained accessible until last Monday, by which time escalating media attention and a petition on Change.org with nearly 5,000 signatures embarrassed administrators into action. For the time it was viewable, the page stigmatized a population far more likely to be attacked than to attack, far less likely to receive justice when injured, and far more likely to be misunderstood. © 2015 The New York Times Company
The month of your birth influences your risk of developing dementia. Although the effect is small compared to risk factors such as obesity, it may show how the first few months of life can affect cognitive health for decades to come. Demographers Gabriele Doblhammer and Thomas Fritze from the University of Rostock, Germany, studied data from the Allgemeine Ortskrankenkasse – Germany’s largest public health insurer – for nearly 150,000 people aged 65 and over. After adjusting for age, they found that those born in the three months from December to February had a 7 per cent lower risk of developing dementia than those born in June to August, with the risk for other months falling in between. There’s nothing astrological about the effect, however. Instead, birth month is a marker for environmental conditions such as weather and nutrition, says Gerard van den Berg, an economist at the University of Bristol, UK, who studies the effects of economic circumstances on health. Summer-born babies are younger when they face the respiratory infections of their first winter, for example. And in the past, babies born in spring and summer would have been in late gestation when the supply of fresh fruit and vegetables from the autumn harvest would have largely run out. Pollution from wood fires or coal heating might also have played a role. There’s evidence from other studies that such factors can have lifelong effects on metabolism and the immune system, increasing the risk of conditions such as diabetes, obesity and high blood pressure. Doblhammer and Fritze’s results show this is true for dementia too. © Copyright Reed Business Information Ltd.
By Bill Berkrot (Reuters) - U.S. researchers on Thursday said they had found a way to predict male sexual orientation based on molecular markers that control DNA function, but genetics experts warned that the research has important limitations and will not provide definitive answers to a potential biological basis for sexual preference. Findings from the study, which has yet to be published or reviewed in detail by other scientists, were presented at a meeting of the American Society of Human Genetics in Baltimore. It followed 37 pairs of identical male twins in which one was homosexual and one heterosexual, and 10 sets of twins in which both males were homosexual. The study found that the presence of specific epigenetic marks in nine areas of the human genome could predict homosexual preference with up to 70% accuracy. The epigenome is sometimes described as molecular "switches" that can turn on or silence individual genes in DNA. Scientists believe epigenetic differences can be influenced by environmental and lifestyle factors, from exposure to chemicals to parental nurturing. "To our knowledge, this is the first example of a predictive model for sexual orientation based on molecular markers," Tuck Ngun, lead researcher on the study from the David Geffen School of Medicine of the University of California, Los Angeles, said in a statement. Genetics experts who critiqued the findings said it was premature to draw any conclusions on the predictive powers of epigenetic markers. © 2015 Scientific American
Gay or straight? A saliva test can predict the answer, and get it right 67 per cent of the time – for male identical twins at least. The test, which uses clues from tiny modifications to a person’s genome, is the first that claims to detect sexual orientation. Many scientists have expressed caution over the results, while concerns over potential misuse of the test have led the study’s lead researcher to quit the project entirely. “The scientific benefit to understanding [why people vary in sexual orientation] is obvious to anyone with an iota of curiosity,” says Michael Bailey at Northwestern University in Evanston, Illinois. “The predictive test needs replication on larger samples in order to know how good it is, but in theory it’s quite interesting.” Over the last two decades, several studies have suggested that sexual orientation is, in part, down to our genes. Perhaps the biggest splash was made in 1993 by Dean Hamer’s team at the National Cancer Institute in Bethesda, Maryland, when they found that gay brothers tended to share a sequence of five genetic markers in a region of the X chromosome. The same region has been implicated in other studies of sexual orientation since, although researchers haven’t been able to single out “gay genes”. Other observations also suggest a genetic basis for sexual orientation, such as the mysterious fraternal birth order effect. For every male pregnancy a woman has, a subsequent son has a 33 per cent higher chance of being homosexual, although no one knows why. The overall chance is still low, however, rising from around 2 per cent to just 6 per cent for a third son. © Copyright Reed Business Information Ltd.
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