Chapter 7. Life-Span Development of the Brain and Behavior
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By PETER GODFREY-SMITH Around 2008, while snorkeling and scuba diving in my free time, I began watching the unusual group of animals known as cephalopods, the group that includes octopuses, cuttlefish and squid. The first ones I encountered were giant cuttlefish, large animals whose skin changes color so quickly and completely that swimming after them can be like following an aquatic, multi-armed television. Then I began watching octopuses. Despite being mollusks, like clams and oysters, these animals have very large brains and exhibit a curious, enigmatic intelligence. I followed them through the sea, and also began reading about them, and one of the first things I learned came as a shock: They have extremely short lives — just one or two years. I was already puzzled by the evolution of large brains in cephalopods, and this discovery made the questions more acute. What is the point of building a complex brain like that if your life is over in a year or two? Why invest in a process of learning about the world if there is no time to put that information to use? An octopus’s or cuttlefish’s life is rich in experience, but it is incredibly compressed. The particular puzzle of octopus life span opens up a more general one. Why do animals age? And why do they age so differently? A scruffy-looking fish that inhabits the same patch of sea as my cephalopods has relatives who live to 200 years of age. This seems extraordinarily unfair: A dull-looking fish lives for centuries while the cuttlefish, in their chromatic splendor, and the octopuses, in their inquisitive intelligence, are dead before they are 2? There are monkeys the size of a mouse that can live for 15 years, and hummingbirds that can live for over 10. Nautiluses (who are also cephalopods) can live for 20 years. A recent Nature paper reported that despite continuing medical advances, humans appear to have reached a rough plateau at around 115 years, though a few people will edge beyond it. The life spans of animals seem to lack all rhyme or reason. © 2016 The New York Times Company
Erika Check Hayden Physicians may soon have a lot more help in treating newborns. Neuroscientists and physicians have embarked on what they hope will be a revolution in treatments to prevent brain damage in newborn babies. As many as 800,000 babies die each year when blood and oxygen stop flowing to the brain around the time of birth. And thousands develop brain damage that causes long-lasting mental or physical disabilities, such as cerebral palsy. Physicians have few tools to prevent this, but they are optimistic that clinical trials now under way will change things. The trials were sparked by neuroscientists’ realization in the 1990s that some brain injuries can be repaired. That discovery spurred a flurry of basic research that is just now coming to fruition in the clinic. In January, a US study will start to test whether the hormone erythropoietin, or EPO, can prevent brain damage hours after birth when combined with hypothermia, in which babies are cooled to 33.5 °C. A trial in Australia is already testing this treatment. Physicians in countries including the United States, China and Switzerland are testing EPO in premature babies, as well as other treatments, such as melatonin, xenon, argon, magnesium, allopurinol and cord blood in full-term babies. “The world has really changed for us,” says neurologist Janet Soul at Boston Children’s Hospital in Massachusetts. Therapeutic hypothermia was the first success: clinical trials over the past decade have shown that it decreases the risk of death and of major brain-development disorders by as much as 60%. It is now standard treatment for babies in developed countries whose brains are deprived of blood and oxygen during birth. © 2016 Macmillan Publishers Limited,
Keyword: Development of the Brain
Link ID: 22935 - Posted: 11.30.2016
By Dwayne Godwin, Jorge Cham © 2016 Scientific American,
Alison Abbott & Elie Dolgin A drug that was seen as a major test of the leading theory behind Alzheimer’s disease has failed in a large trial of people with mild dementia. Critics of the ‘amyloid hypothesis’, which posits that the disease is triggered by a build-up of amyloid protein in the brain, have seized on the results as evidence of its weakness. But the jury is still out on whether the theory will eventually yield a treatment. Proponents of the theory note that the particular way in which solanezumab, the drug involved in the trial, works could have led to the failure, rather than a flaw in the hypothesis itself. And many trials are ongoing to test whether solanezumab — or others that target amyloid — could work in people at risk of the disease who have not yet shown symptoms, or even in people with Alzheimer’s, despite the latest negative result. “I’m extremely disappointed for patients, but this, for me, doesn’t change the way I think about the amyloid hypothesis,” says Reisa Sperling, a neurologist at the Brigham and Women’s Hospital in Boston, Massachusetts. She is leading one of several ongoing ‘prevention’ trials that is testing solanezumab, and other drugs that aim to reduce the build-up of amyloid ‘plaques’, in people at risk of developing Alzheimer’s. Solanezumab is an antibody that mops up amyloid proteins from the blood and cerebrospinal fluid. The proteins can go on to form plaques in the brain. Eli Lilly, the company that developed solanezumab, announced on 23 November that it would abandon the drug as a treatment for patients with mild dementia. The outcome adds to a long list of promising Alzheimer’s drugs that have flopped in the clinic, many of which, like solanezumab, targeted amyloid. © 2016 Macmillan Publishers Limited
Link ID: 22912 - Posted: 11.25.2016
By PAM BELLUCK It is the news that doctors and families in the heart of Zika territory had feared: Some babies not born with the unusually small heads that are the most severe hallmark of brain damage as a result of the virus have developed the condition, called microcephaly, as they have grown older. The findings were reported in a study of 13 babies in Brazil that was published Tuesday in Morbidity and Mortality Weekly Report. At birth, none of the babies had heads small enough to receive a diagnosis of microcephaly, but months later, 11 of them did. For most of those babies, brain scans soon after birth showed significant abnormalities, and researchers found that as the babies aged, their brains did not grow or develop enough for their age and body size. The new study echoes another published this fall, in which three babies were found to have microcephaly later in their first year. As they closed in on their first birthdays, many of the babies also had some of the other developmental and medical problems caused by Zika infection, a range of disabilities now being called congenital Zika syndrome. The impairments resemble characteristics of cerebral palsy and include epileptic seizures, muscle and joint problems and difficulties swallowing food. “There are some areas of great deficiency in the babies,” said Dr. Cynthia Moore, the director of the division of congenital and developmental disorders for the Centers for Disease Control and Prevention and an author of the new study. “They certainly are going to have a lot of impairment.” Dr. Deborah Levine, a professor of radiology at Harvard Medical School who has studied Zika but was not involved in either study, said there would most likely be other waves of children whose brains were affected by the Zika infection, but not severely enough to be noticed in their first year. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 22903 - Posted: 11.23.2016
Laura Sanders Harmful factors circulating in old blood may be partly responsible for the mental decline that can come with age, a small study in mice suggests. Irina Conboy of the University of California, Berkeley and colleagues devised a new way to mingle blood in two mice that didn’t involve stitching their bodies together, as in previous experiments (SN: 5/31/14, p. 8). Instead, researchers used a microfluidic device to shuttle blood, a process that precisely controlled the timing and amount of blood transferred between the mice. The method, reported online November 22 in Nature Communications, allows more precise tests of blood’s influence on aging, the researchers believe. Old mice benefited in some ways from infusions of young blood, experiments with four young-old pairs of mice revealed. With young blood around, old muscles were better able to recover after an injury. And young blood seemed to improve old livers in some tests. But young blood didn’t seem to help one measure of brain health. After transfusions of young blood, old mice still had lower numbers of newborn nerve cells in the hippocampus, a brain structure important for learning and memory. What’s more, old blood reduced the number of newborn nerve cells in young mice. This damage happened quickly, after just one blood exchange, the researchers found. The results suggest that old blood contains components that harm brain cells, an insight that makes scientists eager to identify those factors. |© Society for Science & the Public 2000 - 2016
Keyword: Development of the Brain
Link ID: 22898 - Posted: 11.23.2016
By GINA KOLATA Despite fears that dementia rates were going to explode as the population grows older and fatter, and has more diabetes and high blood pressure, a large nationally representative survey has found the reverse. Dementia is actually on the wane. And when people do get dementia, they get it at older and older ages. Previous studies found the same trend but involved much smaller and less diverse populations like the mostly white population of Framingham, Mass., and residents of a few areas in England and Wales. The new study found that the dementia rate in Americans 65 and older fell by 24 percent over 12 years, to 8.8 percent in 2012 from 11.6 percent in 2000. That trend is “statistically significant and impressive,” said Samuel Preston, a demographer at the University of Pennsylvania who was not associated with the study. In 2000, people received a diagnosis of dementia at an average age of 80.7; in 2012, the average age was 82.4. “The dementia rate is not immutable,” said Dr. Richard Hodes, director of the National Institute on Aging. “It can change.” And that “is very good news,” said John Haaga, director of the institute’s division of behavioral and social research. It means, he said, that “roughly a million and a half people aged 65 and older who do not have dementia now would have had it if the rate in 2000 had been in place.” Keith Fargo, director of scientific programs and outreach at the Alzheimer’s Association, said the group had been encouraged by some of the previous research showing a decline but had also been “a little bit nervous” about drawing conclusions because the populations in the earlier studies were so homogeneous. Now, he said of the new data, “here is a nationally representative study. It’s wonderful news.” © 2016 The New York Times Company
Link ID: 22896 - Posted: 11.22.2016
By JAN HOFFMAN BOWLING GREEN, Ky. — Crosby J. Gardner has never had a girlfriend. Now 20 and living for the first time in a dorm here at Western Kentucky University, he has designed a fast-track experiment to find her. He ticks off the math. Two meals a day at the student dining hall, three courses per meal. Girls make up 57 percent of the 20,068 students. And so, he sums up, gray-blue eyes triumphant, if he sits at a table with at least four new girls for every course, he should be able to meet all 11,439 by graduation. “I’m Crosby Gardner!” he announces each time he descends upon a fresh group, trying out the social-skills script he had practiced in the university’s autism support program. “What is your name and what is your major?” The first generation of college students with an autism diagnosis is fanning out to campuses across the country. These growing numbers reflect the sharp rise in diagnosis rates since the 1990s, as well as the success of early-learning interventions and efforts to include these students in mainstream activities. But while these young adults have opportunities that could not have been imagined had they been born even a decade earlier, their success in college is still a long shot. Increasingly, schools are realizing that most of these students will not graduate without comprehensive support like the Kelly Autism Program at Western Kentucky. Similar programs have been taking root at nearly 40 colleges around the country, including large public institutions like Eastern Michigan University, California State University, Long Beach, the University of Connecticut and Rutgers. For decades, universities have provided academic safety nets to students with physical disabilities and learning challenges like dyslexia. But students on the autism spectrum need a web of support that is far more nuanced and complex. © 2016 The New York Times Company
Link ID: 22894 - Posted: 11.21.2016
Nicola Davis Smart bottles that dispense the correct dose of medication at the correct time, digital assistants, and chairs that know how long you’ve sat in them are among the devices set to change the face of care for those living with dementia. Dementia is now the leading cause of death in England and Wales, and is thought to affect more than 850,000 people in the UK. But a new wave of connected devices, dubbed “the internet of things”, could offer new ways to help people live independently for longer. “We have got an elderly population, and children in their 40s and 50s are looking after their elderly parents – and they may not have the capabilities to coordinate that care effectively,” said Idris Jahn, head of health and data at IoTUK, a programme within the government-backed Digital Catapult. While phone calls and text messages help to keep people in touch, says Jahn, problems can still arise, from missed appointments to difficulties in taking medication correctly. But he adds, connected sensors and devices that collect and process data in real time could help solve the problem. “For [people living with dementia] the sensors would be more in the environment itself, so embedded into the plug sockets, into the lights – so it is effectively invisible. You carry on living your life but in the background things will monitor you and provide feedback to people who need to know,” he said. “That might be your carer, it might be your family, it might be your clinician.” The approach, he added, has the potential to change the way care is given. “It is having that cohesive mechanism to put everyone into the loop, which I think hasn’t existed in the past and it is something that people need.” © 2016 Guardian News and Media Limited
Link ID: 22887 - Posted: 11.19.2016
Laura Sanders SAN DIEGO — Mice raised in cages bombarded with glowing lights and sounds have profound brain abnormalities and behavioral trouble. Hours of daily stimulation led to behaviors reminiscent of attention-deficit/hyperactivity disorder, scientists reported November 14 at the annual meeting of the Society for Neuroscience. Certain kinds of sensory stimulation, such as sights and sounds, are known to help the brain develop correctly. But scientists from Seattle Children’s Research Institute wondered whether too much stimulation or stimulation of the wrong sort could have negative effects on the growing brain. To mimic extreme screen exposure, mice were blasted with flashing lights and TV audio for six hours a day. The cacophony began when the mice were 10 days old and lasted for six weeks. After the end of the ordeal, scientists examined the mice’s brains. “We found dramatic changes everywhere in the brain,” said study coauthor Jan-Marino Ramirez. Mice that had been stimulated had fewer newborn nerve cells in the hippocampus, a brain structure important for learning and memory, than unstimulated mice, Ramirez said. The stimulation also made certain nerve cells more active in general. Stimulated mice also displayed behaviors similar to some associated with ADHD in children. These mice were noticeably more active and had trouble remembering whether they had encountered an object. The mice also seemed more inclined to take risks, venturing into open areas that mice normally shy away from, for instance. |© Society for Science & the Public 2000 - 2016.
By Jessica Hamzelou Having an agile mind in your 90s might sound like wishful thinking, but some people manage to retain youthful memories until their dying days. Now post mortems have revealed that these “superagers” manage to do this even when their brains have the hallmarks of Alzheimer’s diseases. Superagers have the memory and cognition of the average person almost half their age, and manage to avoid Alzheimer’s symptoms. Aras Rezvanian at Northwestern University in Chicago, Illinois, and his colleagues have been looking at brain samples donated by such people to try to understand what their secret might be. The group looked at eight brains, all from people who had lived into their 90s, and had memory and cognition scores of the average 50-year-old until their final days. Specifically, the team studied two brain regions – the hippocampus, which is involved in memory, and the prefrontal cortex, which is key for cognition. They found that the brain samples of the superagers had plaques and tangles in them to varying degrees. These are sticky clumps and twisted fibres of protein that seem to be linked to the death of neurons, and are usually found in the brains of people with Alzheimer’s disease after they die. Of the eight superager samples, two had such a high density and distribution of these proteins that they resembled the most severe cases of Alzheimer’s. © Copyright Reed Business Information Ltd.
Link ID: 22868 - Posted: 11.15.2016
Tom Siegfried SAN DIEGO — Babies as young as 5 months old possess networks of brain cell activity that react to facial emotions, especially fear, a new study finds. “Networks for recognizing facial expressions are in place shortly after birth,” Catherine Stamoulis of Harvard Medical School said November 13 during a news conference at the annual meeting of the Society for Neuroscience. “This work … is the first evidence that networks that are involved in a function that is critical to survival, such as the recognition of facial expressions, come online very early in life.” Stamoulis and colleagues at Harvard and Boston Children’s Hospital analyzed a database of brain electrical activity collected from 58 infants as they aged from 5 months to 3 years. Brain activity was measured as the infants viewed pictures of female faces expressing happiness, anger or fear. Computer models of the brain activity showed that networks responding to fear were activated much more dramatically than those for happy or angry faces, even in the youngest infants. As babies grew older, their brain networks responding to facial emotions became less complex as redundant nerve cell connections were pruned. But the fear network remained more complex than the others, and response to fearful faces remained elevated over time. Understanding the brain circuitry involved in responding to emotional facial expressions could have implications for research on developmental disorders, Stamoulis said. |© Society for Science & the Public 2000 - 2016.
Kathleen Taylor The global rise in dementia should surprise no one. The figures — such as the 9.9 million new diagnoses each year — have been known for decades. As slow as we are to accept such vast changes on a personal, societal and political level, so research is slow to uncover why our brains become fragile with age. Neuroscientist and writer Kathleen Taylor's The Fragile Brain is about that research. But it is much more than a simple reflection on the best published hypotheses. Taylor has crafted a personal, astonishingly coherent review of our current state of knowledge about the causes of Alzheimer's disease and dementia, as well as possible solutions, from lifestyle adjustments to drug developments. Filled with elegant metaphors, her study covers the detail of molecular biology and larger-scale analysis, including epidemiological observations and clinical studies. It extends to dementia due to multiple sclerosis, stroke and encephalitis. For instance, some 5–30% of people who have a first stroke develop dementia. But the book's focus is Alzheimer's disease, and rightly so: it is what up to 80% of people with dementia are diagnosed with. Taylor begins with a shocking juxtaposition, setting the costs of age-related disorders and of dementia alongside the scarcity in funding. In Britain, Australia and the United States, for example, funding for dementia research is a fraction of that for cancer — in the United States, just 18%. She contextualizes with reflections on the history of dementia research, deftly unravelling the roles of pioneering scientists Alois Alzheimer, Franz Nissl and Emil Kraepelin in describing the condition. © 2016 Macmillan Publishers Limited,
Elie Dolgin There are not a lot of things that could bring together people as far apart on the US political spectrum as Republican Newt Gingrich and Democrat Bob Kerrey. But in 2007, after leading a three-year commission that looked into the costs of care for elderly people, the political rivals came to full agreement on a common enemy: dementia. At the time, there were fewer than 30 million people worldwide diagnosed with the condition, but it was clear that the numbers were set to explode. By 2050, current predictions suggest, it could reach more than 130 million, at which point the cost to US health care alone from diseases such as Alzheimer’s will probably hit US$1 trillion per year in today’s dollars. “We looked at each other and said, ‘You know, if we don’t get a grip on Alzheimer’s, we can’t get anything done because it’s going to drown the system,’” recalls Gingrich, the former speaker of the US House of Representatives. He still feels that sense of urgency, and for good reason. Funding has not kept pace with the scale of the problem; targets for treatments are thin on the ground and poorly understood; and more than 200 clinical trials for Alzheimer’s therapies have been terminated because the treatments were ineffective. Of the few treatments available, none addresses the underlying disease process. “We’re faced with a tsunami and we’re trying to deal with it with a bucket,” says Gingrich. But this message has begun to reverberate around the world, which gives hope to the clinicians and scientists. Experts say that the coming wave can be calmed with the help of just three things: more money for research, better diagnostics and drugs, and a victory — however small — that would boost morale. © 2016 Macmillan Publishers Limited
Link ID: 22848 - Posted: 11.09.2016
Anesthesia during early childhood surgery poses little risk for intelligence and academics later on, the largest study of its kind suggests. The results were found in research on nearly 200,000 Swedish teens. School grades were only marginally lower in kids who'd had one or more common surgeries with anesthesia before age 4, compared with those who'd had no anesthesia during those early years. Whether the results apply to sicker children who have riskier surgeries with anesthesia is not known. But the researchers from Sweden's Karolinska Institute and doctors elsewhere called the new results reassuring, given experiments in young animals linking anesthesia drugs with brain damage. Previous studies of children have been relatively small, with conflicting results. The new findings, published Monday in JAMA Pediatrics, don't provide a definitive answer and other research is ongoing. The study authors and other doctors say the harms from postponing surgery must be considered when evaluating any potential risks from anesthesia in young children. The most common procedures in the study were hernia repairs; ear, nose or throat surgeries; and abdominal operations. The researchers say the operations likely lasted an hour or less. The study did not include children with other serious health problems and those who had more complex or risky operations, including brain, heart and cancer surgeries. The research involved about 33,500 teens who'd had surgery before age 4 and nearly 160,000 who did not. ©2016 CBC/Radio-Canada.
By Jessica Boddy Glasses may be trendy now, but for centuries they were the stodgy accessories of the elderly worn only for failing eyes. Now, new research suggests that aging bonobos might also benefit from a pair of specs—not for reading, but for grooming. Many older bonobos groom their partners at arm’s length instead of just centimeters away, in the same way that older humans often hold newspapers farther out to read. This made researchers think the apes might also be losing their close-up vision as they age. To see whether their hypothesis held, the researchers took photos of 14 different bonobos of varying ages as they groomed one another (above) and measured the distance between their hands and faces. By analyzing how this so-called grooming distance varied from ape to ape, the researchers found that grooming distance increased exponentially with age, they report today in Current Biology. And because both humans and bonobos shows signs of farsightedness around age 40, deterioration in human eyes might not be the mere result of staring at screens and small text, the scientists say. Rather, it might be a deep-rooted natural trait reaching back to a common ancestor. © 2016 American Association for the Advancement of Science.
Link ID: 22841 - Posted: 11.08.2016
By Marian Vidal-Fernandez, Ana Nuevo-Chiquero, The title of this article might trigger self-satisfied smiles among first-borns, and some concerns among the rest of us. Many studies show children born earlier in the family enjoy better wages and more education, but until now we didn’t really know why. Our recently published findings are the first to suggest advantages of first born siblings start very early in life—around zero to three years old! We observe parents changing their behaviour as new children are born, and offering less cognitive stimulation to children of higher birth order. It now seems clear that for those born and raised in high-income countries such as the United States, the UK and Norway, earlier-born children enjoy higher wages and education as adults—known as the “birth order effect”. Comparing two siblings, the greater the difference in their birth order, the greater the relative benefit to the older child. However, to date we’ve had no evidence that explains where such differences come from. We know it’s not an effect of family size, because the effect remains when comparing siblings within the same family and families with the same number of children. While it makes sense that parents earn more money and gain experience as they get older and have more children, they also need to divide their economic resources and attention among any children that arrive after the first born. We wondered where in childhood these differences began, and what the cause or causes might be. © 2016 Scientific American,
By Simon Makin Cerebral autopsy specimen of a patient diagosed having Alzheimer Disease. In the HE stain numerous plaque formations within the neuropil background are visible. Credit: WIKIPEDIA, CC BY-SA 3.0 On Monday Pres. Barack Obama proclaimed November “National Alzheimer's Disease Awareness Month.” The administration’s ambitious goal is to prevent and treat Alzheimer's by 2025. Although there are currently no approved therapies that slow or stop progression of the disease, several approaches are showing promise. In a study published today in Science Translational Medicine, a team from Merck Research Laboratories reports results of early human and animal trials of a drug called verubecestat, which targets the production of protein plaques associated with the disease. “It's a summary of the discovery and early-stage profiling of what we hope is going to be a new therapeutic for Alzheimer's,” says team leader Matthew Kennedy. “It represents well over a decade of investment in this project by many, many scientists.” Definitive conclusions will have to await the results of larger, ongoing phase III clinical trials to assess their efficacy, effectiveness and safety, but the results are promising, experts say. Verubecestat is a so-called BACE1 inhibitor. BACE1 (for Beta-site Amyloid precursor protein Cleaving Enzyme 1, aka beta-secretase 1) is an enzyme involved in producing amyloid beta (Ab), a protein that clumps together, eventually forming the plaques surrounding neurons that are the disease's key hallmark. The amyloid hypothesis of Alzheimer's proposes that the accumulation of amyloid beta aggregates in the brain drives a cascade of biological events leading to neurodegeneration. By blocking BACE1, the hope is this approach could prevent the buildup of these clumps in the first place. But until now, development of these drugs has been hindered by problems finding molecules with the right characteristics, and concerns over theoretical and actual side effects. © 2016 Scientific American
Link ID: 22827 - Posted: 11.03.2016
Bruce Bower Many preschoolers take a surprisingly long and bumpy mental path to the realization that people can have mistaken beliefs — say, thinking that a ball is in a basket when it has secretly been moved to a toy box. Traditional learning curves, in which kids gradually move from knowing nothing to complete understanding, don’t apply to this landmark social achievement and probably to many other types of learning, a new study concludes. Kids ranging in age from 3 to 5 often go back and forth between passing and failing false-belief tests for several months to more than one year, say psychologist Sara Baker of the University of Cambridge and her colleagues. A small minority of youngsters jump quickly from always failing to always passing these tests, the scientists report October 20 in Cognitive Psychology. “If these results are replicated, it will surprise a lot of researchers that there is such a low level of sudden insight into false beliefs,” says psychologist Malinda Carpenter, currently at the Max Planck Institute for Evolutionary Anthropology in Leipzig. Early childhood researchers generally assume that preschoolers either pass or fail false-belief tests, with a brief transition between the two, explains Carpenter, who did not participate in the new study. Grasping that others sometimes have mistaken beliefs is a key step in social thinking. False-belief understanding may start out as something that can be indicated nonverbally but not described. Human 2-year-olds and even chimpanzees tend to look toward spots where a person would expect to find a hidden item that only the children or apes have seen moved elsewhere (SN Online: 10/6/16). © Society for Science & the Public 2000 - 2016
By Jesse Singal For a long time, the United States’ justice system has been notorious for its proclivity for imprisoning children. Because of laws that grant prosecutors and judges discretion to bump juveniles up to the category of “adult” when they commit crimes deemed serious enough by the authorities, the U.S. is an outlier in locking up kids, with some youthful defendants even getting life sentences. Naturally, this has attracted a great deal of outrage and advocacy from human-rights organizations, who argue that kids, by virtue of not lacking certain judgment, foresight, and decision-making abilities, should be treated a bit more leniently. Writing for the Marshall Project and drawing on some interesting brain science, Dana Goldstein takes the argument about youth incarceration even further: We should also rethink our treatment of offenders who are young adults. As Goldstein explains, the more researchers study the brain, the more they realize that it takes decades for the organ to develop fully and to impart to its owners their full, adult capacities for reasoning. “Altogether,” she writes, “the research suggests that brain maturation continues into one’s twenties and even thirties.” Many of these insights come from the newest generation of neuroscience research. “Everyone has always known that there are behavioral changes throughout the lifespan,” Catherine Lebel, an assistant professor of radiology at the University of Calgary who has conducted research into brain development, told Goldstein. “It’s only with new imaging techniques over the last 15 years that we’ve been able to get at some of these more subtle changes.” ! © 2016, New York Media LLC.