Chapter 7. Life-Span Development of the Brain and Behavior
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
Brain cell regeneration has been discovered in a new location in human brains. The finding raises hopes that these cells could be used to help people recover after a stroke, or to treat other brain diseases. For years it was unclear whether or not we could generate new brain cells during our lifetime, as the process – neurogenesis – had only been seen in animals. Instead, it was thought that humans, with our large and complex brains, are born with all the required neurons. Then last year Jonas Frisén of the Karolinska Institute in Stockholm, Sweden, and his colleagues found that neurogenesis occurs in the hippocampi of the human brain. These structures are crucial for memory formation (Cell, DOI: 10.1016/j.cell.2013.05.002) Now they have found more new brain cells in a second location – golf-ball-sized structures called the striata. These seem to be involved in many different functions, including in learning and memory. These particular aspects, related as they are to the hippocampi, lead Frisén to speculate that these new brain cells may also be involved with learning. "New neurons may convey some sort of plasticity," he says, which might help people learn and adapt to new situations. To reveal the new brain cells, the team exploited the fact that there have been varying levels of a radioactive isotope of carbon – carbon-14 – in the atmosphere since nuclear bomb tests during the cold war. This means that the year of creation of many cells in the body can be found by measuring the ratio of carbon-14 to carbon-12 in its DNA. Analysis of 30 donated brains revealed which brain cells had been born during the lifetimes of the donors. © Copyright Reed Business Information Ltd.
Link ID: 19282 - Posted: 02.22.2014
National Institutes of Health researchers have identified gene variants that cause a rare syndrome of sporadic fevers, skin rashes and recurring strokes, beginning early in childhood. The team’s discovery coincides with findings by an Israeli research group that identified an overlapping set of variants of the same gene in patients with a similar type of blood vessel inflammation. The NIH group first encountered a patient with the syndrome approximately 10 years ago. The patient, then 3 years old, experienced fevers, skin rash and strokes that left her severely disabled. Because there was no history of a similar illness in the family, the NIH group did not at first suspect a genetic cause, and treated the patient with immunosuppressive medication. However, when the NIH team evaluated a second patient with similar symptoms two years ago — a child who had experienced recurrent fevers and six strokes by her sixth birthday — they began to suspect a common genetic cause and embarked on a medical odyssey that has led not only to a diagnosis, but to fundamental new insights into blood vessel disease. In their study, which appears in the Feb. 19, 2014, advance online edition of the New England Journal of Medicine, the researchers describe how next-generation genome sequencing, only recently available, facilitated a molecular diagnosis for patients in their study. The researchers found that harmful variants in the CECR1 gene impede production of a protein vital to the integrity of healthy blood vessel walls. The researchers showed that faulty variants in their patients’ DNA that encode the CECR1 gene cause a loss of function of the gene’s ability to produce of an enzyme called adenosine deaminase 2 (ADA2). Without it, abnormalities and inflammation in blood vessel walls result. The researchers call the new syndrome, deficiency of ADA2, or DADA2.
Ian Sample, science correspondent, in Chicago Regular brisk walks can slow down the shrinking of the brain and the faltering mental skills that old age often brings, scientists say. Studies on men and women aged 60 to 80 found that taking a short walk three times a week increased the size of brain regions linked to planning and memory over the course of a year. The prefrontal cortex and hippocampus increased in size by only 2% or 3%, but that was enough to offset the steady shrinkage doctors expected to see over the same period. "It may sound like a modest amount but that's actually like reversing the age clock by about one to two years," said Professor Kirk Erickson, a neuroscientist at the University of Pittsburgh. "While the brain is shrinking, we actually saw not a levelling out but an increase in the size of these regions. It was better than before we started the study." People who took part in the study scored higher on spatial memory tests, and some reported feeling more mentally alert, according to Erickson. "They feel better, they feel as if the fog has lifted. Anecdotally, it seems to benefit these cognitive functions," he said. Erickson recruited more than 100 adults who confessed to doing little if any exercise in their daily lives. Half were randomly assigned to walk for 30 to 45 minutes three days a week. The rest spent a similar amount of time doing stretching exercises. Medical scans showed minor increases in the two brain regions in both groups. But the effect was greater in the walkers, Erickson said at the annual meeting of the American Association for the Advancement of Science. © 2014 Guardian News and Media Limited
Link ID: 19271 - Posted: 02.20.2014
By ALAN SCHWARZ Jerry, 9 years old, dissolved into his Game Boy while his father described his attentional difficulties to the family pediatrician. The child began flitting around the room distractedly, ignoring the doctor’s questions and squirming in his chair — but then he leapt up and yelled: “Freeze! What do you think is the problem here?” Nine-year-old Jerry was in fact being played by Dr. Peter Jensen, one of the nation’s most prominent child psychiatrists. On this Sunday in January in New York, Dr. Jensen was on a cross-country tour, teaching pediatricians and other medical providers how to properly evaluate children’s mental health issues — especially attention deficit hyperactivity disorder, which some doctors diagnose despite having little professional training. One in seven children in the United States — and almost 20 percent of all boys — receives a diagnosis of A.D.H.D. by the time they turn 18, according to the Centers for Disease Control and Prevention. It narrowly trails asthma as the most common long-term medical condition in children. Increasing concern about the handling of the disorder has raised questions about the training doctors receive before diagnosing the condition and prescribing stimulants like Adderall or Concerta, sometimes with little understanding of the risks. The medications can cause sleep problems, loss of appetite and, in rare cases, delusions. Because the disorder became a widespread national health concern only in the past few decades, many current pediatricians received little formal instruction on it, sometimes only several hours, during their seven years of medical school and residency. But the national scarcity of child psychiatrists has placed much of the burden for evaluating children’s behavioral problems on general pediatricians and family doctors, a reality that Dr. Jensen and others are trying to address through classes that emphasize role-playing exercises and spirited debate. © 2014 The New York Times Company
By GRETCHEN REYNOLDS Watching participants in slopestyle and half-pipe skiing and snowboarding flip, curl, cartwheel and otherwise contort themselves in the air during the Winter Olympics competition, many of us have probably wondered not only how the athletes managed to perform such feats but also why. Helpfully, a recent study of the genetics of risk-taking intimates that their behavior may be motivated, at least in part, by their DNA. For some time, scientists and many parents have suspected that certain children are born needing greater physical stimulation than others, suggesting that sensation seeking, as this urge is known in psychological terms, has a genetic component. A thought-provoking 2006 study of twins, for instance, concluded that risk-taking behavior was shared by the pairs to a much greater extent than could be accounted for solely by environmental factors. If one twin sought out risks, the other was likely to do so as well. But finding which genes or, more specifically, which tiny snippets of DNA within genes, might be influencing the desire to huck oneself off of a snow-covered slope has proven to be troublesome. In recent years, scientists zeroed in on various sections of genes that affect the brain’s levels of or response to the neurotransmitter dopamine, a substance that is known to influence our feelings of pleasure, reward and gratification. People who engage in and enjoy extreme, daredevil conduct, researchers presumed, would likely process dopamine differently than those of us content to watch. But the results of some early genetic studies comparing dopamine-related portions of genes with sensation seeking were inconsistent. Some found that people with certain variations within genes, including a gene called DRD4 that is believed to be closely involved in the development and function of dopamine receptors in our brain, gravitated toward risky behavior. Others, though, found no such links. But most of these studies focused on so-called deviant risk-taking, such as gambling and drug addiction. © 2014 The New York Times Company
By Geoffrey Mohan Stress can damage the brain. The hormones it releases can change the way nerves fire, and send circuits into a dangerous feedback loop, leaving us vulnerable to anxiety, depression and post-traumatic stress disorder. But how stress accomplishes its sinister work on a cellular level has remained mysterious. Neuroscientists at a UC Berkeley lab have uncovered evidence that a well-known stress hormone trips a switch in stem cells in the brain, causing them to produce a white matter cell that ultimately can change the way circuits are connected in the brain. This key step toward hardening wires, the researchers found, may be at the heart of the hyper-connected circuits associated with prolonged, acute stress, according to the study published online Tuesday in the journal Molecular Psychiatry. The findings strengthen an emerging view that cells once written off as little more than glue, insulation and scaffolding may regulate and reorganize the brain's circuitry. Researchers examined a population of stem cells in the brain’s hippocampus, an area critical to fusing emotion and memory, and one that has been known to shrink under the effects of prolonged acute stress. Under normal circumstances, these cells form new neurons or glia, a type of white matter. Los Angeles Times Copyright 2014
Ian Sample, science correspondent, in Chicago A woman's diet in early life has more impact on her baby's birth weight than the food she eats as an adult, researchers say. The surprise finding suggests that you are what your mother ate, and that a woman's diet in her adult life has less influence on her baby's health than previously thought. Prof Christopher Kuzawa at Northwestern University in Illinois said that women's bodies seemed to "buffer" the supply of nutrients to their unborn babies, meaning that foetuses were partly protected from changes in women's diets. Kuzawa advised pregnant women to follow a healthy diet, but said they need not worry about every calorie because their health and diet as a toddler could be more important for their baby. "There is some good news here for expectant mothers. Although there certainly are some harmful things to avoid during pregnancy, and some supplements to take to make sure some important bases are covered, the mother's body seems to do a good job of buffering overall nutritional supply to her growing baby," he said. "Within the bounds of a healthy balanced diet, the overall quantity of food that a mother eats is unlikely to have large effects on her baby's birth weight," he added. The findings emerged from a 30-year study that followed more than 3,000 pregnant women in the Philippines whose children have now begun to have babies of their own. Kuzawa said that while there was good evidence that unborn children benefit from their mothers taking extra folate and that they are harmed by toxins such as lead, mercury, excessive alcohol and bisphenol A, which is used to make some plastics, the picture was less clear on the roles of calories, protein, fat and carbohydrates. © 2014 Guardian News and Media Limited
by Ashley Yeager Humans aren’t the only ones to suffer from obsessive-compulsive disorder. Dogs can suffer from the disorder as well, with particular breeds compulsively chewing their feet, chasing their tails or sucking blankets. Now scientists say they have identified several of the genes that trigger the behavior in Doberman pinschers, bullterriers, sheepdogs and German shepherds. Four genes, CDH2, CTNNA2, ATXN1 and PGCP, involved in the communication between brain cells appear to play a role in dog OCD, researchers report February 16 in Genome Biology. The results could be used to better understand the disorder in people. © Society for Science & the Public 2000 - 2013.
Kids with ADHD may be able to learn better focus through a computer game that trains the brain to pay attention, a new study suggests. The game was part of a neurofeedback system that used bicycle helmets wired to measure brain waves and gave immediate feedback when kids were paying attention, researchers reported Monday in Pediatrics. Giving kids feedback on what their brains are doing is "like turning on a light switch," said Dr. Naomi Steiner, the study's lead author and a developmental and behavioral pediatrician at the Floating Hospital for Children at Tufts Medical Center. "Kids said 'Oh, this is what people mean when they tell me to pay attention.'" To test the system, Steiner and her colleagues randomly assigned 104 Boston area elementary school children to one of three groups: no treatment, 40 half-hour sessions of neurofeedback or 40 sessions of cognitive therapy. The kids getting neurofeedback wore standard bicycle helmets fitted with brain wave sensors while they performed a variety of exercises on the computer. In one exercise, kids were told to focus on a cartoon dolphin. When people pay attention, theta wave activity goes down while beta waves increase, Steiner explained. If the kids' brains showed they were paying attention, the dolphin would dive to the bottom of the sea. Parents' reports on ADHD symptoms six months later showed a lasting improvement in kids who had done neurofeedback.
CHICAGO, ILLINOIS—Chances are, your baby won’t respond to questions like, “How was your day, honey?” Or, “What do you want to be when you grow up?” But just because infants can’t form sentences until toddlerhood doesn’t mean that they don’t benefit from early conversations with their parents. It’s long been observed that the better children perform in school and the more successful their careers, the higher the socioeconomic status (SES) of their family—and, according to Stanford University’s Anne Fernald, this has a lot to do with how parents of different SES speak to their babies. Those babies that are spoken to frequently in an engaging and nurturing way—generally from a higher SES—tend to develop faster word-processing skills, or the ability to follow a sentence from one object or setting to another. This word processing speed, in turn, directly relates to the development not just of vocabulary and language skills, but also memory and nonverbal cognitive abilities. In a new study, Fernald and colleagues measured parent-baby banter from round-the-clock recordings in babies’ homes, then tested those babies’ word-processing speed using retinal-following experiments that tracked how long it took them to follow a prompt to an image like a dog or juice. The researchers found that the differences in word-processing speed between high and low SES were stark: By 2 years of age, high SES children were 6 months ahead of their low SES counterparts; and by age 3, the differences in processing abilities were highly predictive of later performance in and out of school, the team reported here today at the annual meeting of AAAS, which publishes Science. Fernald hopes that this research will lead to interventions that help to shrink the language gap between kids on either side of the income gap. © 2014 American Association for the Advancement of Science
by Laura Sanders Some of the human brain’s wrinkles are forged by the behavior of a single gene, scientists report in the Feb. 14 Science. By scanning more than 1,000 people’s brains, researchers identified five with malformed wrinkles in a specific region. The abnormalities — numerous shallow dips surrounding an unusually wide brain furrow called the Sylvian fissure — were linked with intellectual and language disabilities and seizures in these people. All five people had mutations that dampened the behavior of a gene named GPR56. Curbing this gene’s behavior results in diminished production of cells that eventually become neurons in the affected brain region, mouse experiments revealed. Boosting the gene’s behavior had the opposite effect. The results might clarify how wrinkles allow human brains to cram lots of neurons into a small space, Christopher Walsh of Boston Children’s Hospital and colleagues suggest. © Society for Science & the Public 2000 - 2013
|By Dina Fine Maron Concussions are a major problem in football. But brain injury is a growing concern in soccer, too, usually resulting from heading the ball or collisions. A meta-analysis of existing studies finds that concussions accounted for between 6 and 9 percent of all injuries sustained on soccer fields. Most of those concussions come from when two players make for the ball, often when a player’s elbow, arm or hand inadvertently makes contact with another player’s head. But we’re not just talking about injuries to professionals. One work shows some 63 percent of all varsity soccer players have sustained concussions—yet only 19 percent realized it. And another says girls’ soccer can be particularly brutal, accounting for 8 percent of all sports-related concussions among high school girls. The findings are in the journal Brain Injury. [Monica E. Maher et al., Concussions and heading in soccer: A review of the evidence of incidence, mechanisms, biomarkers and neurocognitive outcomes] Professional players who reported a great deal of extensive heading the ball during their careers did the poorest in tests of verbal and visual memory compared with other players. Goalies and defenders were most likely to get concussions. So if you want to bend it like Beckham, maybe focus on playing midfield or offense. Padding the goal posts would also be a heads-up policy. © 2014 Scientific American
by Bethany Brookshire There are times when science is a painful experience. My most excruciating moment in science involved a heated electrode placed on my bare leg. This wasn’t some sort of graduate school hazing ritual. I was a volunteer in a study to determine how we process feelings of pain. As part of the experiment I was exposed to different levels of heat and asked how painful I thought they were. When the electrode was removed, I eagerly asked how my pain tolerance compared with that of others. I secretly hoped that I was some sort of superwoman, capable of feeling pain that would send other people into screaming fits and brushing it off with a stoic grimace. It turns out, however, that I was a bit of a wuss. Ouch. I figured I could just blame my genes. About half of our susceptibility to pain can be explained by genetic differences. The other half, however, remains up for grabs. And a new study published February 4 in Nature Communications suggests that part of our susceptibility to pain might lie in chemical markers on our genes. These “notes” on your DNA, known as epigenetic changes, can be affected by environment, behavior and even diet. So the findings reveal that our genetic susceptibility to pain might not be our destiny. Tim Spector and Jordana Bell, genetic epidemiologists at King’s College London, were interested in the role of the epigenome in pain sensitivity. Epigenetic changes such as the addition (or subtraction) of a methyl group on a gene make that gene more or less likely to be used in a cell by altering how much protein can be made from it. These differences in proteins can affect everything from obesity to memory to whether you end up like your mother. © Society for Science & the Public 2000 - 2013.
|By Annie Sneed Alzheimer’s disease is now the sixth leading cause of death in the U.S., but researchers still do not know what causes the degenerative neurological disorder. In recent years they have pinpointed several genes that seem largely responsible for those cases in which the disorder develops early on, prior to age 60. They have also identified about 20 genes that can increase or decrease risk for the more common late-onset variety that starts appearing in people older than 60. But genetics simply cannot explain the whole picture for the over five million Americans with late-onset Alzheimer’s. Whereas genetics contribute some risk of developing this version of the disorder, no combination of genes inevitably leads to the disease. Scientists are now urgently searching for the other missing pieces to explain what causes late-onset Alzheimer’s. Some researchers have shifted their attention from genes to the environment—especially to certain toxins. Their studies of pesticides, food additives, air pollution and other problematic compounds are opening a new front in the battle against this devastating malady. Here’s a roundup of some of the possibilities being studied: Scientists have already found a strong potential link between pesticides and Parkinson’s disease. Now, a preliminary study released in January suggests that the pesticide DDT, which degrades so slowly that it continues to linger in the environment more than 40 years after the U.S. Environmental Protection Agency banned its use in the U.S., may also contribute to Alzheimer’s. © 2014 Scientific American
By Maggie Fox Researchers looking for simple ways to treat autism say they may have explained why at least some cases occur: It all has to do with the stress babies undergo at birth. They’re already testing a simple drug for treating kids with autism and say their findings may point to ways to treat the disorder earlier in life. It’s all experimental, but the study, published in the journal Science, should inspire other researchers to take a closer look. “This is exciting stuff to people in the field, because it’s getting at a basic mechanism," says Andrew Zimmerman of the University of Massachusetts Medical School, who reviewed the study. Yehezkel Ben-Ari of the Mediterranean Institute of Neurobiology in Marseille, France, and colleagues have been treating children with autism with a diuretic called bumetanide that reduces levels of chloride in cells. Diuretics lower blood pressure by making people urinate more, reducing fluid. Ben-Ari has had mixed success in his trials in kids, and wanted to prove his theory that chloride was the key. He worked with two rodent “models” of autism — they’re the closest things scientists have for replicating autism in a human. One has mutated genes linked with autism, and another develops autism when given valproate, an epilepsy drug blamed for causing autism in the children of mothers who take it while pregnant. They looked at what was going on in the brains of the mouse and rat pups just before and after birth. Then they gave the mouse and rat moms bumetanide — and fewer of their newborns showed autistic-like behaviors.
Ewen Callaway A study in mice and rats suggests that an imbalance in chloride ions during a child's development in the womb could be a factor for autism. Children with autism typically begin showing obvious symptoms, such as trouble making eye contact and slow language development, a year or more after birth. A study in mice and rats now hints that prenatal drug treatment could head off these problems. The findings, reported today in Science1, do not suggest that autism spectrum disorders can be prevented in children. But researchers not involved in the study say that they add support to a controversial clinical trial suggesting that some children with autism benefited from taking a common diuretic medication called bumetanide2. In that trial, a team led by neuroscientist Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille gave 60 children bumetanide or a placebo daily for three months. Children who had less severe forms of autism showed mild improvements in social behaviour after taking the drug, and almost no adverse side effects were observed (see 'Diuretic drug improves symptoms of autism'). But autism researchers greeted the results with caution. Many pointed out that the study did not provide a clear biological mechanism that could explain how the drug improved the symptoms of the disorder. The latest study is an attempt to answer such criticisms by identifying a role for the neurotransmitter GABA. Studies in humans and animals have suggested that GABA, which in healthy people typically inhibits the activity in neurons, is altered in autism and instead activates some brain cells. © 2014 Nature Publishing Group,
Link ID: 19225 - Posted: 02.08.2014
By NICHOLAS BAKALAR There are many well established risk factors for cardiovascular death, but researchers may have found one more: slower reaction time. In the late 1980s and early ’90s, researchers measured the reaction times of 5,134 adults ages 20 to 59, having them press a button as quickly as possible after a light flashed on a computer screen. Then they followed them to see how many would still be alive after 15 years. The study is in the January issue of PLOS One. Unsurprisingly, men, smokers, heavy drinkers and the physically inactive were more likely to die. But after controlling for these and other factors, they found that those with slower reaction times were 25 percent more likely to die of any cause, and 36 percent more likely to die of cardiovascular disease, than those with faster reactions. Reaction time made no difference in cancer mortality. The reasons for the connection are unclear, but the lead author, Gareth Hagger-Johnson, a senior research associate at University College London, said it may reflect problems with the brain or nervous system. He stressed, though, that “a single test of reaction time is not going to tell you when you’re going to die. There’s a link at a population level. We didn’t look at individual people.” © 2014 The New York Times Company
Keyword: Development of the Brain
Link ID: 19210 - Posted: 02.06.2014
|By Geoffrey Giller Working memory—our ability to store pieces of information temporarily—is crucial both for everyday activities like dialing a phone number as well as for more taxing tasks like arithmetic and accurate note-taking. The strength of working memory is often measured with cognitive tests, such as repeating lists of numbers in reverse order or recalling sequences of dots on a screen. For children, performance on working memory assessments is considered a strong predictor for future academic performance. Yet cognitive tests can fail to identify children whose brain development is lagging in subtle ways that may lead to future deficits in working memory and, thus, in learning. Doctors give the tests periodically and plot the results along a development curve, much like a child’s height and weight. By the time these tests reveal that a child’s working memory is below average, however, it may be too late to do much about it. But in a new study, published January 29 in The Journal of Neuroscience, scientists demonstrated that they could predict the future working memory of children and adolescents by examining brain scans from two different types of magnetic resonance imaging (MRI), instead of looking only at cognitive tests. Henrik Ullman, a PhD student at the Karolinska Institute in Stockholm and the lead author on the paper, says that this was the first study attempting to use MRI scans to predict future working memory capacity. “We were pretty surprised when we found what we actually found,” Ullman says. © 2014 Scientific American,
by Andy Coghlan If you flinch where others merely frown, you might want to take a look at your lifestyle. That's because environmental factors may have retuned your genes to make you more sensitive to pain. "We know that stressful life events such as diet, smoking, drinking and exposure to pollution all have effects on your genes, but we didn't know if they specifically affected pain genes," says Tim Spector of King's College London. Now, a study of identical twins suggests they do. It seems that epigenetic changes – environmentally triggered chemical alterations that affect how active your genes are – can dial your pain threshold up or down. This implies that genetic tweaks of this kind, such as the addition of one or more methyl groups to a gene, may account for some differences in how our senses operate. Spector and his colleagues assessed the ability of hundreds of pairs of twins to withstand the heat of a laser on their skin, a standard pain test. They selected 25 pairs who showed the greatest difference in the highest temperature they could bear. Since identical twins have the same genes, any variation in pain sensitivity can be attributed to epigenetic differences. Pain thermostat The researchers screened the twins' DNA for differences in methylation levels across 10 million gene regions. They found a significant difference in nine genes, most of which then turned out to have been previously implicated in pain-sensitivity in animal experiments. © Copyright Reed Business Information Ltd.
One thing marijuana isn’t known to do is improve your memory. But there’s another reason why scientists believe it could fight Alzheimer’s disease. Gary Wenk, PhD, professor of neuroscience, immunology and medical genetics at Ohio State University, has studied how to combat brain inflammation for over 25 years. His research has led him to a class of compounds known as cannabinoids, which includes many of the common ingredients in marijuana. He says, throughout all of his research, cannabinoids have been the only class of drugs he’s found to work. What’s more, he believes early intervention may be the best way of fighting Alzheimer’s. Dr. Wenk doesn’t see cannabinoids – or anything else – as a cure. But he took the time to discuss with us how marijuana might prevent the disorder from developing. Q: What’s so important about brain inflammation? Over the past few years, there’s been a focus on inflammation in the brain as causing a lot more than Alzheimer’s. We now know it plays a role in ALS, Parkinson’s disease, AIDS, dementia, multiple sclerosis, autism, schizophrenia, etc. We’re beginning to see that inflammation in the brain, if it lasts too long, can be quite detrimental. And if you do anything, such as smoke a bunch of marijuana in your 20s and 30s, you may wipe out all of the inflammation in your brain and then things start over again. And you simply die of old age before inflammation becomes an issue for you. © 2013-2014 All rights reserved